Scientific studies on Camel urine

ScientificstudiesonCamelurine
http://caller-to-islam.tk

Camel urine components display anti-cancer properties in vitro
Nujoud Al-Yousef a
, Ameera Gaafar b
, Basem Al-Otaibi c
, Ibrahim Al-Jammaz c
,
Khaled Al-Hussein b
, Abdelilah Aboussekhra a,n
a
Department of Molecular Oncology, King Faisal Specialist Hospital and Research Center, MBC # 03, PO BOX 3354, Riyadh 11211, Saudi Arabia
b
Histocompatibility & Immunogenetics Research Unit, Stem Cell Therapy Program, King Faisal Specialist Hospital and Research Center, MBC # 03, PO BOX 3354,
Riyadh 11211, Saudi Arabia
c
Department of Cyclotron and Radiopharmaceuticals, King Faisal Specialist Hospital and Research Center, MBC # 03, PO BOX 3354, Riyadh 11211, Saudi Arabia
a r t i c l e i n f o
Article history:
Received 17 March 2012
Received in revised form
23 July 2012
Accepted 27 July 2012
Available online 16 August 2012
Keywords:
Camel urine
Cancer
Apoptosis
Immune response
a b s t r a c t
Ethnopharmacological relevance: While camel urine (CU) is widely used in the Arabian Peninsula to
treat various diseases, including cancer, its exact mechanism of action is still not defined. The objective
of the present study is to investigate whether camel urine has anti-cancer effect on human cells in vitro.
Materials and methods: The annexinV/PI assay was used to assess apoptosis, and immunoblotting
analysis determined the effect of CU on different apoptotic and oncogenic proteins. Furthermore, flow
cytometry and Elispot were utilized to investigate cytotoxicity and the effect on the cell cycle as well as
the production of cytokines, respectively.
Results: Camel urine showed cytotoxicity against various, but not all, human cancer cell lines, with only
marginal effect on non-tumorigenic epithelial and normal fibroblast cells epithelial and fibroblast cells.
Interestingly, 216 mg/ml of lyophilized CU inhibited cell proliferation and triggered more than 80% of
apoptosis in different cancer cells, including breast carcinomas and medulloblastomas. Apoptosis was
induced in these cells through the intrinsic pathway via Bcl-2 decrease. Furthermore, CU down-
regulated the cancer-promoting proteins survivin, b-catenin and cyclin D1 and increased the level of
the cyclin-dependent kinase inhibitor p21. In addition, we have shown that CU has no cytotoxic effect
against peripheral blood mononuclear cells and has strong immuno-inducer activity through inducing
IFN-g and inhibiting the Th2 cytokines IL-4, IL-6 and IL-10.
Conclusions: CU has specific and efficient anti-cancer and potent immune-modulator properties in vitro.
& 2012 Elsevier Ireland Ltd. All rights reserved.
1. Introduction
Cancer remains a worldwide public health concern. Although
cancer incidence has increased over the past four decades, mortality
has remained stable. This is probably reflecting the improvement in
treatment options. Chemotherapy is a core modality for the treat-
ment of a wide range of cancer types at different stages. However,
most of the currently used chemotherapeutic regimens are highly
toxic with long term side effects, morbidity and lethality (Rood et al.,
2004; Rossi et al., 2008). Of 121 prescription drugs in use for cancer
treatment, 90 are derived from plant species and 74% of these drugs
were discovered by investigating a folklore claim (Craig, 1997;
Craig and Beck, 1999). Among the natural products in the Arabic
peninsula that are used for the treatment of various diseases is
camel urine. Patients drink camel urine ($100 mL/day) either alone
or mixed with milk. This prompted us to ask whether the urine of
this extraordinary animal has anticancer properties? Camel urine
urine has an unusual and unique biochemical composition. Indeed,
Dr. Bernard Read published in 1925 a paper describing the chemical
constituents of camel (Camelus bactrinus) urine (Read, 1925). He
has reported that unlike all the other animals, including humans,
camels excrete no ammonia and only very slight trace of urea, and
these molecules are responsible for bad smell and toxicity of urine.
However, a significant amount of creatine and creatinine was
detected. Further studies have shown that camel urine contains
about 10 folds more mineral salts than human urine. Furthermore,
while human urine is acidic, camel urine is basic with a pHZ7.8
(Read, 1925). In a recent report, Alhaidar et al. have shown that
camel urine has potent antiplatelet activity against ADP-induced
(clopidogrel-like) and AA-induced (aspirin-like) platelet aggregation
(Alhaidar et al., 2011). Several have claimed anti-cancer effects of
camel urine. However, no clear scientific evidence has been pub-
lished so far to confirm or refute these claims. Recently, it has been
shown that camel urine inhibits the induction of Cyp1a1, a cancer
activating gene, in Hepa 1c1c7 cell line (Alhaider et al., 2011). In the
present report we have shown that camel urine has indeed several
anti-cancer properties in vitro.
Contents lists available at SciVerse ScienceDirect
journal homepage: www.elsevier.com/locate/jep
Journal of Ethnopharmacology
0378-8741/$ - see front matter & 2012 Elsevier Ireland Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.jep.2012.07.042
n
Correspondence to: Department of Molecular Oncology, King Faisal Specialist
Hospital and Research Center, MBC # 03-66, PO BOX 3354, Riyadh 11211, Saudi
Arabia. Tel.: þ966 1 464 7272x32840; fax: þ966 1 442 7858.
E-mail address: aboussekhra@kfshrc.edu.sa (A. Aboussekhra).
Journal of Ethnopharmacology 143 (2012) 819–825

2. Materials and methods
2.1. CU preparation and use
Urine was collected aseptically from three young (3–4 years
old) female camels (Camelus dromadaries), desert living healthy
local red ones, in sterile bottles and urine from each camel was
pooled separately. CU was lyophilized, weighted and immediately
before utilization it was resuspended in PBS. Chemical character-
ization of these samples has been performed using 1
H-NMR
analysis using DMSO as solvent system. The obtained spectra
indicate that these CU samples are of the same nature, and
chemical shifts are as follow:
CU1: 1
H-NMR (DMSO, 298 K) d: 7.85 (d), 7.52 (d), 7.46 (t), 7.27
(d), 7.04 (s), 3.66 (s), 3.35 (s), 2.91 (s), 2.50 (s).
CU2: 1
H-NMR (DMSO, 298 K) d: 7.86 (d), 7.47 (d), 7.46 (t), 7.28
(d), 7.04 (s), 3.66 (s), 3.35 (s), 2.91 (s), 2.50 (s).
CU3: 1
H-NMR (DMSO, 298 K) d: 7.85 (d), 7.48 (d), 7.46 (t), 7.28
(d), 7.03 (s), 3.66 (s), 3.34 (s), 2.91 (s), 2.50 (s).
These results were confirmed by HPLC, which shows a major
peak at around 11 min retention time for the 3 samples (Fig. 1).
2.2. Cell lines and cell culture
MCF 10A, MDA-MB-231, U2OS, DAOY, LoVo and HCT-116 were
obtained from ATCC and were cultured following the instructions
of the company. MED-1, MED-8, MED-13 are primary medullo-
blastoma cells that were cultured as previously described
(Shinwari et al., 2011). HFSN1 cells are primary skin fibroblast
cells that were routinely cultured in the DMEM:F12 (50:50)
medium supplemented with 10% FBS.
2.3. Cellular lysate preparation
Cells were washed and scraped in lysis buffer [150 mM NaCl, 1%
NP40, 50 mM Tris–HCl (pH 7.5)] supplemented with 40 mg/ml
aprotinin, 20 mg/ml leupeptin and 5 mg/ml pepstatin. Lysates were
homogenized using a Polytron homogenizer and then centrifuged at
14000 rpm in an Eppendorf microcentrifuge tube for 20 min. The
supernatant was removed, aliquoted and stored at À80 1C.
2.4. Immunoblotting
SDS-PAGE was performed using 12% separating minigels as
previously described (Al-Hujaily et al., 2011). The antibodies
directed against b-Actin (C-11), GAPDH (FL-335), Bax (B-9), Bcl-
2 (C-2), survivin (C-19), p21 (F-5), and p53 (DO-1), b-Catenin
(9F2) and Cyclin D1 (HD11) were purchased from Santa Cruz
Biotechnology, Santa Cruz, CA, USA. The antibodies against
cleaved caspase3 (Asp175), cleaved caspase9 (Asp315) and
cleaved PARP (Asp214) were purchased from Cell Signaling.
2.5. Quantification of protein expression level
The expression levels of the immunoblotted proteins were
measured using the densitometer (BIO-RAD GS-800 Calibrated
Densitometer). X-ray films were scanned and protein signal
intensity of each band was determined. Next, dividing the
obtained value of each band by the values of the corresponding
internal control allowed a correction of the loading differences.
The fold of induction in the protein levels was determined by
dividing the corrected values that corresponded to the treated
samples by that of the non-treated one (time 0).
2.6. Annexin V and flow cytometry
For each cell culture, cells were either not treated (control) or
treated with CU. Detached and adherent cells were then har-
vested after 72 h, unless otherwise stated, and treated as pre-
viously described (Al-Hujaily et al., 2011). For each cell culture
3 independent experiments were performed using 104
cells in
each experiment.
2.7. PBMC preparation and culture
10 ml of heparinised blood samples were obtained from healthy
volunteer employers and then peripheral blood mononuclear
Fig. 1. HPLC analysis of CU samples, 3 camel urine samples (CU1, CU2, CU3) were
analyzed by HPLC and the corresponding chromatograms are shown.
N. Al-Yousef et al. / Journal of Ethnopharmacology 143 (2012) 819–825820

cells (PBMCs) were obtained by centrifugation over ficol-hypaque
gradients (Pharmacia, Uppsala, Sweden). 106
cells were cultured in
RPMI-1640 medium supplemented with 10% FCS (Gibco, Island NY,
PBS) and complements and incubated at 37 1C in 5% CO2 incubator.
2.8. PBMC cytotoxicity
PBMCs were treated with different concentrations of CU for 3 days
and cell death was measured with annexinV/PI-flow cytometry.
2.9. Elispot assay
Elispot assay (Diaclone Research, France) was used as recom-
mended by the manufacturer. 5.103
cells suspended in 100 ml
complete media containing CU (16 mg/mL) and IL-2 and were
incubated for 10 days in 96-well microtiter plates pre-coated with
the appropriate antibody. Subsequently, cells were either treated
with PHA (10 mg/ml) or LPS (1 mg/ml), for stimulating the produc-
tion of IFN-g, IL-4 and IL-10 and IL-6, respectively. The plates
were incubated at 37 1C in humidified atmosphere containing 5%
CO2 for appropriate period of time according to the different
cytokine kinetics. After washing, the plates were read using the
Elispot AID reader version 3.0.
2.10. Cell proliferation analysis
2–4.103
cells were seeded in 96 well plate and 100 ml of
complete medium was loaded in each well. The plate was
incubated for at least 30 min in a humidified, 37 1C, 5% CO2
incubator, and then was inserted into the Real-Time Cell Electro-
nic Sensing System (RT-CES system) (ACEA Biosciences Inc.,
San Diego, CA) for 16 h. Cells were then either PBS-treated or
treated with CU (16 mg/mL) and cell proliferation was monitored
for 24 h.
2.11. HPLC analysis
HPLC analysis was carried out on Econosil C-18 reversed phase
column (analytical, 250 mm Â 4.6 mm). The solvent system used
was non-linear gradient (eluent A, water with 0.1% TFA; eluent B,
ACN; gradient, 0–10% B, 10–90% B, 90–90% B and 90–0% B over
5 min each at flow rate of 1.0 mL/min). A Jasco chromatographic
system equipped with a variable wavelength ultraviolet monitor
and in tandem with a Canberra flow through radioactivity
detector was used. Ultraviolet absorption was monitored at
254 nm. Chromatograms were acquired and analyzed using
BORWIN software.
Fig. 2. CU is cytotoxic against cancer cells but not against normal fibroblasts and non-tumorigenic epithelial cells. Cells were treated with CU as indicated and the cytotoxic effect
was assessed by flow cytometry following PI staining. (A) Cells were treated with the indicated CU doses for 72 h. (B) Cells were treated with CU (16 mg/mL) for the indicated periods
of time. (C and D) The indicated cells were treated with CU (16 mg/mL) for 72 h. (C) Flow cytometry charts. (D) Histogram, Error bars represent means7S.D. *: p valueo0.05.
N. Al-Yousef et al. / Journal of Ethnopharmacology 143 (2012) 819–825 821

2.12. Statistical analysis
Statistical analysis was performed by student’s t-test and p
values of 0.05 and less were considered as statistically significant.
3. Results
3.1. Camel urine is cytotoxic against various cancer cells
We started this study by investigating the cytotoxic effect of CU
against the MDA-MB-231 breast cancer cells as well as the non-
tumorigenic breast epithelial cells (MCF 10A), using the Propidium
Iodide (PI)/flow cytometry technique. Cells were treated with increas-
ing concentrations of CU for 72 h. Fig. 2A shows dose-dependent
increase in the proportion of death cells among MDA-MB-231 cells,
more than 80% died in response to 16 mg/ml ($800 ml of urine). On
the other hand, the same concentrations of CU had no effect on MCF
10A cells. Next, we investigated the effect of CU over time using
16 mg/ml. Fig. 2B shows that the effect of CU on breast cancer cells
increased with time reaching its maximum at 72 h of treatment,
while no effect was observed on MCF 10A cells. This shows that CU is
cytotoxic, but with specific effect on breast cancer cells.
Next, we investigated the specific cytotoxic effect of CU on
other cancer cell lines. Fig. 1C shows that based on the response
to CU, these cells can be grouped into 2 different sub-groups.
Group 1 contains CU-resistant cells including MCF 10A and the
normal fibroblast (HFSN-1) cells, as well as the osteosarcoma
(U2OS), the breast cancer (MCF-7), the medulloblastoma MED-8
and the colon cancer (LoVo and HCT-116) cells. The second group
is composed of CU-sensitive cells, with more than 50% cell death,
and includes the breast cancer (MDA-MB-231) and the medullo-
blastoma (DAOY, MED-4 and MED-13) cells (Figs. 2C, 1D). Inter-
estingly, these effects were obtained with similar doses of urine
collected from 2 other female camels (data not shown), indicating
that these CU samples collected from different animals living in
different regions and receiving different foods have similar
chemical characteristics (materials and methods) and cytotoxic
effect against cancer cells. Therefore, CU powders from these
camels were pooled and used in the next experiments.
3.2. Camel urine triggers apoptosis in cancer cells
In order to identify the cell death pathway that CU triggers in
cancer cells, we first made use of the AnnexinV-PI/flow cytometry
technique that can detect both apoptotic and necrotic cells. Fig. 3
Fig. 3. CU induces apoptosis through the mitochondrial pathway. Cells were treated either with PBS or with CU (16 mg/mL) for 72 h, and then cell death was assessed by
annexin V/PI in association with flow cytometry. (A) Charts, the numbers into the boxes indicate the proportion of normal (lower, left), early apoptotic (lower, right), late
apoptotic (higher, right) and necrotic (higher, left) cells. (B) Histograms presenting the proportions of induced apoptosis in the indicated normal and cancer cells. Error bars
represent standard deviations of three different experiments, *: p valueo0.05. (C) MDA-MB-231 cells were treated with CU (16 mg/mL), and then were harvested after the
indicated periods of time. 50 mg of extracted proteins were used for western blot analysis utilizing the indicated antibodies. The numbers below the bands represent the
corresponding expression levels as compared to time 0 and after normalization against GAPDH. D. As in C, b-actin was used as internal control and the graph is showing
the Bax/Bcl-2 ratios after normalization against b-actin. Error bars represent standard deviations of three different experiments.

shows that CU treatment (16 mg/mL) for 72 h triggered mainly
apoptosis (90%) with only slight proportion of necrosis. Interest-
ingly, the efficiency of CU in inducing apoptosis was variable
among the various cancer cells. While the medulloblastoma DAOY
and MED-4 cells showed high sensitivity, MED-8 showed clear
resistance (Fig. 3B). Interestingly, Fig. 3 confirmed what has been
shown in Fig. 2 for the sensitive cells. However, for the resistant
ones, the annexin V assay showed higher proportion of cells dying
through the apoptotic pathway.
To confirm the induction of apoptosis, MDA-MB-231 cells were
treated with CU (16 mg/mL) and harvested after different periods
of time (0–72 h). Whole cell extracts were prepared and 50 mg of
proteins were used to analyze the effect of CU on the cleavage of
the important effector caspase 3 by immunoblotting. Fig. 3C
shows that treatment by CU caused a time-dependent increase
in the level of the active cleaved caspase 3, reaching at 72 h a level
18.6 fold higher than the basal level. Similarly, the level of cleaved
PARP increased 3.4 fold as compared to the basal level after 48 h
of treatment (Fig. 3C). Together, these results clearly show that
CU triggers apoptosis in MDA-MB-231 cells.
3.3. Camel urine triggers apoptosis via the mitochondrial pathway
Next, we evaluated the effect of CU on the levels of the pro-
and anti-apoptotic proteins (Bax and Bcl-2). Fig. 3D shows that CU
triggered a time-dependent decrease in the level of the anti-
apoptotic protein Bcl-2 and a time-dependent increase in the
level of the pro-apoptosis protein Bax. This led to a time-
dependent increase in the Bax/Bcl-2 ratio, reaching its maximum
(3 fold higher) after 72 h of treatment (Fig. 3D). This shows that
CU induces apoptosis mainly through the mitochondrial pathway
via Bcl-2 decrease. To confirm this we assessed the effect of CU on
the level of caspase 9 and cleaved caspase 9. Fig. 3C shows that
while the level of caspase 9 decreased 5 fold, a strong increase in
the level of cleaved caspase 9 was observed, which confirms the
induction of the apoptotic mitochondrial pathway by CU. Further-
more, CU also decreased the expression of the anti-apoptotic
survivin protein, reaching a level more than 33 fold lower after
72 h of treatment (Fig. 3C).
3.4. Camel urine efficiently inhibits the proliferation of breast cancer
cells
Next, we used the Real-Time Cell Electronic Sensing System to
study the effect of CU on MCF 10A and MDA-MB-231 cell
proliferation. Therefore, cells were cultured for 16 h and then
were treated either with PBS or with CU (16 mg/mL) and were
reincubated for 24 h during which their proliferation rate was
assessed. Fig. 4 shows that while PBS-treated MDA-MB-231 and
CU-treated MCF 10A cells continued to proliferate normally, the
proliferation rate of CU-treated MDA-MB-231 cells decreased
sharply and cells stopped proliferating immediately after adding
CU. This shows that CU has great anti-proliferative effect on
breast cancer cells.
3.5. Effect of camel urine on cancer-related genes
MDA-MB-231 cells were treated with CU (16 mg/mL) for
different periods of time (0–24 h), and then protein levels were
monitored by immunoblotting. Interestingly, CU significantly
down-regulated b-catenin, which reached a level 5 fold lower
after 16 h of treatment (Fig. 5). To confirm the inhibitory effect of
CU on b-catenin, we studied the effect of CU on its major target
cyclin D1 (Rowlands et al., 2004). Indeed, the level of cyclin D1
decreased also more than two fold after 24 h of treatment (Fig. 5).
In addition, CU decreased by 2 fold the level of survivin (Fig. 4).
Together, these results show that CU inhibits the b-catenin-
related cancer pathway. Furthermore, CU up-regulated the
expression of the cyclin-dependent kinase inhibitor p21, with a
maximum level (3.5 fold higher) reached after 16 h of treatment
(Fig. 5).
3.6. Camel urine is not cytotoxic against blood cells and is a potent
modulator of the immune system
We first studied the cytotoxic effect of CU on peripheral blood
mononuclear cells (PBMCs) obtained from healthy individuals.
Cells were treated with increasing CU concentrations, incubated
for 6 h and then cell viability was assessed using AnnexinV/PI
flow cytometry. Fig. 6A shows that CU was not cytotoxic against
PBMCs. At high concentration (20 mg/mL) the viability decreased
to about 45%. However, the level of CD3 did not decrease by
increasing the CU dose. This indicates that the proportion of T
cells did not change, showing that CU does not affect these
important population of immune cells. Moreover, the CU acti-
vated these cells as indicated by the increase of the CD3þ
CD69þ
and CD3þ
HLA-DRþ
. This activation was more pronounced at the
high dose of 20 mg/mL (Fig. 6A).
Next, we evaluated the effect of CU on the immunogenecity of
PBMCs from normal controls. Interestingly, treatment of PBMCs
with CU (20 mg/mL) stimulated the production of IFN-g, which
reached a level 25 fold higher than that of resting PBMCs (Fig. 6B).
Fig. 4. CU inhibits cell proliferation. Sub-confluent cells were treated either with
PBS or with CU (16 mg/mL) for the indicated periods of time, and cell proliferation
rate was determined using the Real-Time Cell Electronic Sensing System.
Fig. 5. CU modulates the expression of several oncoproteins. MDA-MB-231 cells
were treated with CU (16 mg/mL) for the indicated periods of time. Subsequently,
cells were harvested and 50 mg of extracted proteins were used for western blot
analysis using the indicated antibodies. The numbers under the bands represent
the corresponding expression levels as compared to time 0 and after normal-
ization against GAPDH.

On the other hand, the produced level of IL-6 was 5 fold reduced
by CU-treatment (Fig. 6B). Furthermore, CU strongly reduced the
production of IL-4 and IL-10, which became almost undetectable.
This indicates that CU is a potent immuno-modulator product.
4. Discussion
An efficient anti-cancer agent is expected to trigger cell death
and/or inhibit cell proliferation of cancer cells avoiding normal
ones, and activates the immune system. In the present report we
present evidence that camel urine collected from 3 different
female camels presents all these features. Indeed, we have first
shown that CU is cytotoxic against different human cancer cell
lines, while it has only marginal effect on normal fibroblasts and
non-tumorigenic epithelial cells. This specific anti-cancer effect
was not observed when cells were exposed to rat urine, which
killed both cancer as well as normal cells with similar effect (data
not shown). Next, we used different techniques to elucidate the
cell death pathway induced by CU, and we have shown that CU
triggers mainly apoptosis through the mitochondrial pathway, via
Bcl-2 decrease. Importantly, cancer cells exhibited differential
response to the killing effect of CU. In fact, U2OS, MED-8, MCF-7
and MED-13 were resistant to CU. Furthermore, even tumors from
the same organ showed different sensitivity to CU. For example,
while the medulloblastoma DAOY cell line and primary cells
MED-4 showed high sensitivity to CU, MED-8 and MED-13 were
resistant to the same dose. Similarly, the breast cancer cell line
MCF7 exhibited high resistance, whilst MDA-MB-231 was highly
sensitive (Fig. 3). This suggests that CU-dependent induction of
apoptosis is genetically regulated. Indeed, we have shown that CU
modulates the expression of several cancer-related genes, such
as b-catenin, cyclin D1 and the anti-apoptotic survivin protein.
b-catenin is a transcription factor that has been found highly
expressed in various types of cancer, including breast carcinomas
(Prasad et al., 2007; Paul and Dey, 2008). Cyclin D1 is an oncogene
that is over-expressed in about 50% of all breast cancer cases
(Bartkova et al., 1995), and its down-regulation is an important
target in breast cancer therapy (Yang et al., 2006). Furthermore,
CU had a strong inhibitory effect on the two major apoptosis
inhibitor proteins Bcl-2 and survivin, which are both related to
breast cancer pathology and therapeutic outcome (Tanaka et al.,
2000; Callagy et al., 2006; Altieri, 2008). Furthermore, it has been
recently shown that CU significantly inhibits the induction of
Cyp1a1, a well known cancer activating gene, in Hepa 1 C7 cell
line (Alhaider et al., 2011). Therefore, CU seems to inhibit cancer
through targeting several molecular signaling pathways.
In addition, CU exhibited potent anti-proliferative effect on
breast cancer cells but not on non-tumor epithelial cells (Fig. 4).
This effect could be mediated through the induction of the cyclin-
dependent kinase inhibitor p21. Indeed, we have shown that CU
up-regulates p21 in the p53-defective MDA-MB-231 cells (Lacroix
et al., 2006), indicating that this effect is p53-independent.
Furthermore, CU enhanced the production of the main Th1
cytokine IFN-g and also has a great inhibitory effect on the
production of the Th2 cytokines IL-4, IL-6 and IL-10, which has
immunosuppressive and tumor growth stimulating functions.
Cumulative evidence indicate that IL-4 is a key cytokine not only
for Th2 type immune reactions but also for tumor cell growth
itself in various human cancers, including breast carcinomas
(Nagai and Toi, 2000). Similarly, high systemic levels of IL-10
correlated well with poor survival of patients suffering from
different types of cancer (Mocellin et al., 2005). The IL-6 cytokine
is a potent growth factor for breast cancer cells. Moreover, high
levels of IL-6 were detected in breast cancer serums and the
increase correlated with the stage of the tumors (Knupfer and
Preiss, 2007). This indicates that IL-6 down-regulation holds
promises as a potential therapeutic strategy to combat breast
cancer.
In conclusion, the present data provide clear indication that
camel urine has anticancer effects on various human cancer cell
lines. Therefore, we are currently searching for the active
molecule(s) present in this natural animal product.
Acknowledgments
We are grateful to the Research Centre Administration for their
continuous support. We also thank P.S. Manogaran for his help
with the flow cytometry, and M. Velasco for his help with the figures.
This work was performed under RAC # 2100018.
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Original Articles
The Antiplatelet Activity of Camel Urine
Abdulqader Alhaidar, BPharm, MSc, PhD,1
Abdel Galil M. Abdel Gader, MD, PhD,1
and Shaker A. Mousa, PhD, MBA1,2
Abstract
Background: For centuries, camel urine has been used for medicinal purposes and anecdotally proclaimed as a
cure for a wide range of diseases. However, the apparent therapeutic actions of camel urine have yet to be
subjected to rigorous scientific scrutiny. Recent preliminary studies from the authors’ laboratory have indicated
that camel urine possesses potent antiplatelet activity, not found in human or bovine urines, suggesting a
possible role for camel urine in inhibiting platelet function. The goal of the current study was to characterize the
antiplatelet activity of camel urine against normal human platelets based on agonist-induced aggregation and
platelet function analyzer (PFA-100) closure time.
Materials and methods: Urine was collected from healthy virgin, pregnant, and lactating camels aged 2–10
years. Platelet-rich plasma (PRP) was prepared from blood collected from healthy individuals’ blood into ci-
trated anticoagulant. Agonist-induced aggregometry using donor PRP and PFA-100 closure times in whole
blood were carried out in the presence and absence of added camel urine. The responses of platelets to multiple
doses of camel urine were also assessed. The experimental procedure was repeated in human and bovine urines.
Results: Camel urine completely inhibited arachidonic acid (AA) and adnosine diphosphate (ADP)–induced
aggregation of human platelets in a dose-dependent manner. PFA-100 closure time using human whole blood
was prolonged following the addition of camel urine in a dose-dependent manner. Virgin camel urine was less
effective in inhibiting ADP-induced aggregation as compared to urine from lactating and pregnant camels; however,
all three showed comparable inhibitory activity. Neither human nor bovine urine exhibited antiplatelet activity.
Conclusions: Camel urine has potent antiplatelet activity against ADP-induced (clopidogrel-like) and AA-
induced (aspirin-like) platelet aggregation; neither human nor bovine urine exhibited such properties. These novel
results provide the first scientific evidence of the mechanism of the presumed therapeutic properties of camel urine.
Introduction
The one-humped camel (Camelus dromedaries) survives
and reproduces under conditions of extreme drought and
heat that are unsustainable to most other species of domestic
mammal. Desert dwellers have used the camel for transpor-
tation and as a source of food, but just as importantly, its milk
and urine have been used as medicines for centuries.1,2
Camel
milk and urine, for example, have been used to treat various
ailments such as cancer,3,4
chronic hepatitis,5
hepatitis C,6,7
and peptic ulcers.8
More recently, it has been reported that
camel milk can be used to successfully treat severe food al-
lergies in children who are unresponsive to more conven-
tional treatments.9
Most of the claimed therapeutic benefits of camel milk
and urine are attributed variously to anti-infective, anti-
inflammatory, and anticancer properties; by comparison,
very little information is available on the efficacy of camel
urine and/or milk in treating cardiovascular diseases. Short-
chain peptides prepared from bovine milk have been shown
to have potent antihypertensive angiotensin-converting en-
zyme inhibitory action, because they can significantly reduce
blood pressure after intravenous or oral administration, but
they show little or no effect in normotensive subjects.10,11
By
contrast, none of the claims of therapeutic benefit of camel
urine or milk have been subjected to rigorous scientific
scrutiny, and as a result, skepticism about camel urine, in
particular as a form of alternative therapy, is strong. Along
with this, there is a severe shortage of information on the
constituents of camel milk and urine.
The authors’ interest in this area stems from recent work
in our laboratory characterizing camel platelets, in which it
1
The Coagulation Research Laboratory, Department of Physiology, College of Medicine and King Khalid University Hospital, King Saud
University, Riyadh, Saudi Arabia.
2
The Pharmaceutical Research Institute, Albany College of Pharmacy and Health Sciences, Rensselaer, NY.
THE JOURNAL OF ALTERNATIVE AND COMPLEMENTARY MEDICINE
Volume 17, Number 9, 2011, pp. 803–808
ª Mary Ann Liebert, Inc.
DOI: 10.1089/acm.2010.0473
803

was demonstrated that the ultrastructure and function of
camel platelets bears a high degree of dissimilarity as com-
pared to human platelets.12,13
In addition, camels exhibited
markedly inhibited platelet function in terms of agonist-
induced aggregation responses and platelet function ana-
lyzer (PFA-100) closure times.12
Notably, the addition of camel
platelet–poor plasma to packed human erythrocytes resulted
in a prolongation of PFA-100 closure time in human blood
samples (Abdul Gader, unpublished observations). These re-
sults suggest that camel plasma has antiplatelet properties.
The authors set out to investigate whether camel urine has
similar antiplatelet activity, perhaps lending credence to the
claims of the therapeutic benefit of camel urine.
The aim of the current study was to characterize the an-
tiplatelet actions of camel urine on normal human platelets
based on agonist-induced aggregation responses and PFA-
100 closure times. Camel urine exhibited potent platelet in-
hibitory activity, blocking both the prostaglandin pathway
(aspirin-like activity) as well as the adenosine diphosphate
(ADP) receptor–mediated pathway (clopidogrel-like activity).
Neither type of activity was detectable in human or bovine
urine. These novel findings offer the first scientific evidence in
support of the putative therapeutic properties of camel urine.
Materials and Methods
Animals and urine collection
Urine was collected from healthy virgin, pregnant, and
lactating domesticated camels (Camelus dromedaries). All
camels were females, aged 2–10 years. The camels were
raised on a private farm, were disease-free, and had free
access to water and camel feed. The collection of urine was
usually carried out during feeding and was performed by
experienced camel attendants. Urine was allowed to flow
directly into stainless steel containers and then transferred to
glass vials. Urine samples were transported to the laboratory
as soon as practical ( < 4 hours) and were stored at - 80°C
until use. Human and bovine urine was collected and stored
in a similar manner.
Collection of human blood for platelet aggregation
and PFA-100 studies
Healthy volunteers were recruited from among blood
donors, staff, medical students, and residents of our institu-
tion. Specific inquiry was made about the ingestion of aspi-
rin, nonsteroidal anti-inflammatory drugs (NSAIDs), and
any form of cold therapy, at least 2 weeks before blood
collection. Whole blood was drawn by clean venipuncture
directly into vacutainer plastic tubes (Terumu Co., Japan)
containing 3.8% (0.129 M) or 3.2% (0.105 M) buffered sodium
citrate to yield a blood:anti-coagulant ratio of 9:1.
Preparation of platelet-rich plasma
and platelet-poor plasma
Platelet-rich plasma (PRP) was obtained by centrifugation
of citrated whole blood at 800–1000 rpm for 5 minutes. PRP
was removed and the remaining sample was subjected to a
second round of centrifugation at 3000 rpm for 10 minutes to
obtain platelet-poor plasma (PPP). The platelet count of PRP
was in the range of 200–300 · 09
/L. PRP was adjusted to a
concentration of 250,000 – 50,000 with PPP.
Platelet aggregometry
The processing of blood samples and agonist-induced
platelet aggregation technique were carried out as previously
described using a Platelet Aggregation ProfileÒ
(PAP-4)
system (BioData, Horsham, PA).14,15
Arachidonic acid (AA)
(BioData) was reconstituted from a lyophilized preparation
of sodium arachidonate using distilled water to yield a
working concentration of 5 mg/mL. ADP (BioData) was re-
constituted from a lyophilized preparation with distilled
water to yield a working concentration of 2 · 10- 4
M. Special
macrocuvettes (8.75 · 50 mm) were used for all experiments.
Briefly, using plastic tips, 0.45 mL of PRP were pipetted into
the cuvette. Raw camel urine (0.05 mL) was added and the
mixture was stirred with a plastic-coated magnetic stirrer for
2 minutes, after which 0.05 mL of the aggregating agent was
added and the recording was started. Aggregation parame-
ters of maximum aggregation (%) versus control (PPP) and
the slope of the aggregation curve were recorded.
PFA-100 closure time
The PFA-100 assay (PFA-100Ò
; Dade Behring, USA) was
carried out as previously described.12
The PFA100 is a device
that measures platelet-related primary hemostasis in citrated
whole blood specimens. It uses two disposable cartridges
fitted with a membrane with central aperture (147 lm)
coated with aggregation agonists (collagen and epinephrine
and collegen and ADP), through which platelets are passed
at high shear rates (5000–6000 s- 1
). The PFA-100Ò
deter-
mines in whole blood the time (in seconds) elapsed from the
start of the test until a platelet plug occludes the aperture.
This time interval is referred to as closure time (CT), and is
an indicator of platelet function (adhesion and aggregation).
The system was programmed to stop recording when the CT
reached ‡ 300 seconds.
Preparation of the test cartridges. The pouch containing
the test cartridges was allowed to warm up to room tem-
perature prior to opening (approximately 15 minutes). After
removal of the cartridges, the pouch was immediately closed
using the reclosable seal. The top foil seal was removed from
the test cartridge and discarded, and then the test cartridge(s)
was placed in the cassette of the PFA-100 and snapped se-
curely into place.
Sample loading. The following steps were performed in
sequence without interruption.
1. The blood sample was mixed by inverting the collection
tube gently by hand 3–4 times. While the cassette con-
taining the test cartridge was held on a flat surface,
800 lL of blood was pipette into the sample reservoir by
dispensing slowly along one of the inside corners. This
reduces the risk of air entrapment in the sample reser-
voir.
2. The cassette with test cartridge containing sample was
placed into the incubation well(s) of the instrument
such that the cassette was flush with the carousel sur-
face, and then recording was started.
The system was programmed to stop recording when the
aperture closed, or 300 seconds, whichever came first.
804 ALHAIDAR ET AL.

Statistical analysis
Data were analyzed using the SSPS program (Version 15).
Differences in means between groups were compared using
the Mann–Whitney test. Analysis of variance was conducted
using the Kruskal–Wallis test. Proportions from two or more
independent groups were compared using either the v2
test
or Fisher’s Exact test, as appropriate. A p-value £ 0.05 was
considered statistically significant.
Results
A comparison of aggregation responses of human PRP
before (control) and after the addition of camel urine to the
aggregation mixture revealed that urine from virgin, lactat-
ing, and pregnant camels significantly inhibited aggregation
responses to both ADP and AA ( p < 0.001) (Fig. 1). Overall,
urine from lactating camels exhibited the most potent
platelet inhibitory activity. However, close examination of
the individual responses showed that in some cases, camel
urine induced a complete block of the aggregation responses
to ADP and AA, while in other cases, it had no effect. To
identify the prevalence of antiplatelet inhibitory activity in
camel urine, a cut-off value was selected for maximum ag-
gregation response of £ 40%. Using this approach, it was
possible to identify more clearly which camel urine had the
most potent antiplatelet activity (Table 1). Urine from lac-
tating camels exhibited the highest inhibitory activity against
ADP-induced aggregation, followed by pregnant camel ur-
ine, while virgin camel urine was the least potent. In terms of
inhibition of AA-induced aggregation, only lactating camel
urine exhibited potent antiplatelet effects.
The antiplatelet activities of camel urine grouped accord-
ing to maximal aggregation response in the presence of ADP
and AA are shown in Table 2. Inhibition of both ADP- and
AA-induced aggregation differed significantly between lac-
tating (50%), pregnant (29.7%), and virgin (22.4%) urine
samples ( p = 0.0151; v2
test). These results indicated that
lactating camel urine is the most potent inhibitor of human
platelet aggregation.
Dose–response AA and ADP-induced aggregation
by camel urine
Serial dilutions (neat, 1:2, 1:4, 1:8) of camel urine samples
that exhibited complete inhibition of either AA- or ADP-
induced aggregation of normal human platelets were pre-
pared and the aggregation protocol was repeated. Dilutions
were added to human PRP before the addition of ADP or
AA. For all samples, there was a clear dose–response effect of
the camel urine such that as the concentration of urine de-
creased, there was a gradual reduction in inhibition of ag-
gregation (Table 3).
The effect of human and bovine urine
on ADP- and AA-induced aggregation
When the platelet aggregometry assay was repeated using
undiluted human (n = 20) and bovine (n = 24) urine, it was
not possible to detect any inhibition of either AA- or ADP-
induced aggregation (data not shown).
The effect of camel urine on PFA-100 closure time
Camel urine samples that caused a complete inhibition
of both ADP- and AA-induced aggregation were diluted
1:10 and 1:20, and then added to human whole blood (Table
4). In the presence of the higher concentration of camel urine
(1:10 dilution), closure times exceed the limit of the recording
(300 second). When the test was repeated with a lower
concentration of urine (1:20 dilution), a significant shortening
of closure times was observed ( p < 0.001) as compared to
FIG. 1. The effect of camel urine (virgin, lactating, and
pregnant) on the aggregation of human platelets in response
to arachidonic acid (Arch) and adenosine diphosphate
(ADP). Data represent means – standard deviation. Max-
imum aggregation is expressed as a percentage of control
(untreated) platelets. Observations by Gader.
Table 1. Antiplatelet Action of Camel Urine Collected from Virgin, Pregnant, and Lactating Animals
on the Aggregation Responses to Adenosine Diphosphate (ADP) and Arachidonic Acid (AA)
of Healthy Human Platelet-Rich Plasma
Maximum aggregation response to ADP Maximum aggregation response to AA
Study group £ 40% > 40% p-Value £ 40% > 40% p-Value
Control (no urine) 0 (0.0) 42 (34.2) < 0.001* 0 (0.0) 42 (39.2) < 0.001*
Virgin camels 14 (25.9) 44 (35.8) 0.2665 26 (37.1) 32 (29.9) 0.4014
Pregnant camels 19 (35.2) 18 (14.6) 0.0038* 18 (25.8) 19 (17.8) 0.2784
Lactating camels 21 (38.9) 19 (15.4) 0.0012* 26 (37.1) 14 (13.1) < 0.001*
Total 54 (100.0) 123 (100.0) 70 (100.0) 107 (100.0)
Results are expressed as percent maximum aggregation response to ADP and AA of healthy human platelet-rich plasma.
Observations by Gader.
*Statistically significant as compared to untreated samples.
ANTIPLATELET ACTIVITY OF CAMEL URINE 805

samples treated with the lower dilutions (mean of < 300)
(Table 4).
Discussion
Urine therapy, or urotherapy, has been in practice since
early historic times. A search of multiple electronic literature
databases yields a plethora of information on the use of ur-
ine, particularly human urine, with claims of successful
treatment of a wide range of human ailments. However, al-
most all the available information can be categorized as al-
ternative medical practice by healers in many countries,
particularly those where the practice of alternative medicine
is prevalent such as India and China, with scant reporting
from the United States, United Kingdom, and other Euro-
pean countries. The perceived success of such therapeutic
efforts by those who believe in the efficacy of urine therapy,
whether through practice or personal experience, has
prompted several books on urine therapy that have found
wide readership.16–18
Many of the books and reports on ur-
otherapy advocate the use of human urine therapy, partic-
ularly using the individual’s own urine.
Despite numerous claims of efficacy, the practice of ur-
otherapy has yet to be subjected to scientific research, and
even in situations where this form of therapy was prescribed
or advised by qualified physicians, there are no studies that
offer scientific support of such a practice. Therefore, at
present, the practice of urine therapy should be viewed as
unorthodox medical practice based primarily on trial and
error, and not a field that has been subjected to rigorous
scientific scrutiny.
There have been a few isolated references to the use of
bovine urine in Tibet and India, and the use of llama urine (a
member of the Camelidae family) in Tibet, Mongolia, and
China.18
The use of camel urine for therapeutic purposes is
practiced widely among tribes that raise camels, both in Asia
and Africa. In the Middle East, there is credible evidence that
Prophet Mohamed advised the use of camel urine for the
treatment of a wide range of disease conditions.1,2
There are
numerous claims of the success of camel urine therapy in the
management of a range of diseases from liver cirrhosis to
skin and hair ailments.17
Cancer is prominent among the
diseases that are reportedly treatable by urine (human and
camel). Recent studies have shown both in vitro (tissue cul-
ture) and in vivo in humans and animals that a component
isolated from camel urine inhibits the growth of cancer cells,
and reduces the size of both primary tumors and secondary
metastases.19,20
To date, there are no reports in the literature of the use of
camel urine to treat cardiovascular disease. The authors were
encouraged to investigate this possibility by recent results
from their laboratory on the structure and function of camel
platelets.12,13
An important finding of this earlier work was
Table 2. Antiplatelet Action of Camel Urine from Virgin, Pregnant, and Lactating Animals Grouped
According to Percent Maximum Aggregation Response to Adenosine Diphosphate (ADP)
and Arachidonic Acid (AA) on Healthy Human Platelet-Rich Plasma
Study groups
Maximum aggregation
response to ADP
Maximum Aggregation
response to AA Virgin camels Pregnant camels Lactating camels
£ 40 £ 40 13 (22.4%) 11 (29.7%) 20 (50.0%)
£ 40 > 40 1 (1.7%) 8 (21%) 1 (2.5%)
> 40 £ 40 13 (22.4%) 7 (18.9%) 6 (15.0%)
> 40 > 40 31 (53.5%) 11 (29.7%) 13 (32.5%)
Total 58 (100.0%) 37 (100.0%) 40 (100.0%)
Results are expressed as percent maximum aggregation response to ADP or AA of healthy human platelet-rich plasma and are grouped to
show inhibition of aggregation in response to a single agent, or both aggregation agents.
Table 3. The Effect of Different Concentrations
of Camel Urine (Neat and Serial Dilutions)
on Adenosine Diphosphate (ADP)– and Arachidonic
Acid–Induced Platelet Aggregation (Expressed
as Maximum Aggregation %) of Healthy
Human Platelet-Rich Plasma
ADP (10 lg) Arachidonic acid
Neat 1:2 Neat 1:2 1:4 1:8
N 18 18 24 24 24 4
Mean 21.2 58.0* 10.4 28.6* 47.9* 58.1*
SD 9.5 9.0 11.3 22.1 20.7 29.1
*p < 0.001 as compared to neat (Wilcoxon rank sum test).
SD, standard deviation.
Table 4. Summary of PFA-100 Closure Times of Human
Whole Blood After the Addition of Camel Urine
(1/10 and 1/20 Dilutions of Camel Urine Samples
that Caused Complete Inhibition of Adenosine
Diphosphate (ADP)– and Arachidonic
Acid–Induced Aggregation)
PFA-ADP-
1/10
PFA-ADP-
1/20
PFA-EPI-
1/10
PFA-EPI-
1/20
Number 3 3 3 3
Mean 276.7 131.3 300 227.3
SD 29.1 27 0 63
Min 244 102 300 188
Max 300 155 300 300
PFA-100, platelet function analyzer; PFA-ADP, collagen/ADP
cartridge; PFA-EPI, collagen/epinephrine cartridge; SD, standard
deviation.
806 ALHAIDAR ET AL.

the putative antiplatelet properties of camel blood. Analysis
of platelet function using the PFA-100 platelet function an-
alyzer demonstrated that camel blood induces a prolonga-
tion of closure time of human blood.12
These results
suggested that camel plasma may have a platelet inhibitory
activity, and that this activity may be recoverable in urine.
In the present study, camel urine displayed significant
platelet inhibitory activity against human blood collected
from healthy volunteers, blocking the aggregation responses
of human platelets to ADP and AA, and inducing a pro-
longation of PFA-100 closure time. A major advantage of
aggregation studies is that they provide information about
the mechanism of action of agents that modulate platelet
aggregation. Thus, inhibition of ADP-induced aggregation
by camel urine can be assumed to occur mostly at the level
of ADP receptors (P2Y12 and P1Y1).21,22
This assumption
is supported by the result of the present authors’ dose–
response studies. The ADP inhibitory action of camel urine,
therefore, resembles that of the widely used antiplatelet
theinopyridine drugs, particularly clopidogrel, which selec-
tively blocks the P2Y12 receptor. However, the possibility
cannot be excluded that camel urine also blocks the second
P2Y1 receptor as well.
The inhibition of AA-induced aggregation by camel urine
resembles that of aspirin, which blocks the prostaglandin
pathway of platelet activation by irreversibly acetylating the
enzyme cycloxygenase.23,24
Whether the action of camel ur-
ine mimics that of aspirin or whether it acts at other sites
along the prostaglandin pathway (e.g., thromboxane A2 re-
ceptors) is open to speculation.
Conclusions
The current results are the first demonstration of the an-
tiplatelet actions of camel urine and provide an important
foundation of scientific evidence for the exploration of camel
urine as a therapeutic antiplatelet agent. There is also the
interesting possibility that the aspirin-like and clopidogrel-
like actions of camel urine may be responsible for some of its
other widely claimed therapeutic benefits. Clearly, continued
study is needed to uncover the chemical nature of the anti-
platelet effects of camel urine. For example, the current re-
sults do not elucidate why the urine of some camels had
significant antiplatelet effects while that of others did not or
elicited only a partial response. The authors’ recent investi-
gations of the proteome of camel urine (unpublished data)
resulted in the identification of three compounds with
known antiplatelet effects: syndecan-4, an antithrombin-
binding cell surface heparan sulphate proteoglycan25
; a-1-
antichymotrypsin26
; and lactoferrin.27
Whether these pro-
teins constitute the platelet inhibitory action of camel urine
remains to be elucidated.
Lastly, the demonstration that camel urine is endowed
with potent antiplatelet activity lends support to the claimed
anticancer effects of camel urine. Numerous studies have
shown that aspirin has growth-inhibitory action against
cancer cells.28–31
This effect of aspirin is hypothesized to be
through the inhibition of tumor angiogenesis, promotion of
apoptosis, or other possible mechanisms. The potent anti-
platelet activity of camel urine demonstrated in the current
study suggests a putative mechanism for the claimed anti-
cancer properties of camel urine.
Acknowledgments
We thank Lugman Gasmel Sid and Mohamed A. Hamid
for technical assistance.
Disclosure Statement
No competing financial interests exist.
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Address correspondence to:
Abdel Galil M. Abdel Gader, MD, PhD
The Coagulation Research Laboratory
Department of Physiology
College of Medicine and King Khalid University Hospital
King Saud University
Riyadh 11461
Saudi Arabia
E-mail: amagader@ksu.edu.sa
808 ALHAIDAR ET AL.

379
RESEARCH OPINIONS IN ANIMAL & VETERINARY SCIENCES
PRINT ISSN 2221-1896, ONLINE ISSN 2223-0343
www.roavs.com
Preliminary pharmacological investigations on camel urine (Camelus
dromedarius)
Salwa M.E. Khogali1
, Samia .H. Abdrahman1
Baragob, A. E. A. 2
and Elhassan A. M3
1
Department of Biochemistry - Central Veterinary Research Lab - Khartoum, Sudan; 2
Department of
pharmaceutics, Karai University, Omdurman, Sudan; 3
Department of Pharmacology - Alrabat University -
Khartoum, Sudan
Abstract
Pharmacological effects of camel urine (CU), its protein precipitate (PP), diluted urine (DU) and chloroformic
extract (CE) were investigated. The PP inhibited the spontaneous movements of the isolated rat duodenum at a dose
rate of 0.1ml/bath. Diluted female camel urine (0.4 ml/bath) or its protein precipitate (0.8 ml/bath) on rat fundus and
rabbit jejunum revealed serotonin like effect which was antagonized by serotonin blocker cypohyptadine (0.2 ml
/bath). In addition crude female camel urine produced transient relaxation on rabbit jejunum followed by increased
contraction on first washing. chloroformic extract produced no effect on rat duodenum, fundus and rabbit jejunum,
whereas rabbit and chick rectum showed slight changes in the frequency and amplitude contractions.
Key words: Pharmacological, Investigation, Camel, Urine
Introduction
Arabian camel urine was standard prescription in
Arab medicine and remains stable for Bedouin natural
remedies to this day, both as diuretic snuff and
delousing hair detergent (Mona, 1989; Kabariti, 1988).
The percentage of use of camel urine among five
nomadic tribes in eastern Sudan were as follows: 72%
use camel urine for internal problems in general, while
52%, 32%, 20% and 32% used it for malaria, ascitis,
dental problems and hair shampoo respectively.
Regarding the sex of the animal, 88% use female urine
whereas only 12% use male urine. Seventy two percent
drink it as pure urine, whereas twenty eight percent mix
it with milk (Ohaj, 1993, 1998). Therapeutic uses of
animal’s urine have a long history as that of human.
Most of the earlier and current studies deal with
pharmacological and therapeutic effects of human urine
(Bersnyski, 1986; Kabariti, 1988; Kroon, 1996; Martha,
2000; Natalie, 2002). No detailed studies were done on
the pharmacology and/or the possible mechanism(s) of
action of animals urine, especially the dromedary.
Regarding the positive results obtained from the
experimental studies (antibacterial, antifungal,
anticarcinogenic, antiparasitic and hepatoprotective), as
reported by Ohaj, 1998; Wisal, 2002; Mona, 2003 and
Salwa, 2005 respectively, necessitate its pharmaco-
logical investigations. In this study the pharmacological
effect of female camel urine (different extracts) were
performed utilizing laboratory animals isolated strips.
Materials and Methods
Camel urine was collected from naturally grazing
animals (normal urination/or by tashweel technique).
Physiological saline solutions (Tyroid’s & Kerb’s) were
prepared according to the method of Kitchen (1984),
CE, PP of she-camel urine: native protein precipitate
was performed by salt saturation using ammonium
sulphate (40%) w/v and DU was obtained by adding
distilled water to the urine in ratio 3:1. Bioassay of
isolated tissues was prepared according to the method
described by Kitchen (1984). Using duodenum and
fundus strips from a Wister albino rats, jejunum and
rectum strips from local rabbits and rectum strips from
15 day old chicks.
Results
A dose of 0.1 ml/bath of camel urine PP abolished
the spontaneous contractions of rat duodenum as shown
in Fig. (1). Female CU and PP at a dose rate of 0.4 and
0.8 ml/bath, respectively however, stimulated the rat
fundus and rabbit jejunum as shown in Fig. 2 and 3.
The stimulant effects were blocked by cyproheptadine
and atropine at a dose of 0.2 and 0.25ml/bath,
respectively.

Khogali et al roavs, 2011, 1(6), 379-381.
380

Khogali et al roavs, 2011, 1(6), 379-381.
381
CU at 0.1 ml/bath completely abolished the
spontaneous contractions of rabbit jejunum. However,
the inhibitory effect was followed by transient
contraction on first washing. The CE showed slight
effect on rabbit and chick rectum strips Fig.4.
Discussion
This study showed that the inherited knowledge of
traditional usage of camel urine for treating various
ailments in Sudan could be a guide for the discovery of
important biological activities which might be of useful
therapeutic effects. Moreover, the scientific evaluation
and identification of the mechanism (s) of action of
camel urine is important for justification of its
employment in modern medicine, in view of its wide
uses in different parts of Sudan and other Arab
countries. The results of the present study demonstrate
important biological activities of the CU, PP, CE and
DU. DU and CU exerted dual effects on the rabbit
jejunum isolated strips. DU stimulated the organ while
CU abolished the spontaneous rhythmicity of the same
organ. Similar findings were reported by Rodenburg
(1937) using human urine. The stimulant effect
appeared to be mediated via muscarinic receptors
stimulation as the effect was blocked by atropine
sulphate (0.25 ml/bath). This is in agreement with
Vicher (1983) and Ali et al. (1991) findings using
extracts of medicinal plants. The addition of PP directly
stimulated rabbit jejunum at 0.8 µl/bath the effect was
blocked by atropine sulphate (0.2 ml/bath) which
suggests acetylcholine-like action. Rat fundus was
markedly stimulated with PP and DU as did serotonin.
The abolishment of the stimulant effects of both urine
forms and 5-Hydroxytryptamine (5-HT) by the addition
of the non-selective serotonin blocker, cyproheptadine,
demonstrated the 5-HT like activity of PP and DU. This
high sensitivity might be due to the fact that rat fundus
was found to be enriched with the 5-HT2B receptors
(Vane, 1957). This has been recently verified as
subtype of the 5-HT2 receptor family by Cox et al.
(1996). The addition of PP to rat duodenum directly
inhibited the myogenic contractions, which may
suggest a direct musclotropic relaxation of smooth
muscles. Similar findings were reported by Guddum
(1955) and Horton (1959) using human urine. CE
produced slight changes on rabbit and chick rectum
rhythm city, however, no effects were observed on
other strips. It can concluded that camel urine
(indifferent forms) can penetrate subepithelially and
induce generation of mast cells with release of chemical
mediators, followed by forceful peristaltic contractions
caused by 5-HT and other newly formed mediators.
References
Ali, M.B., Mohamed, A.H., Salih, W.M. and Homeida,
A.H. 1991. Effect of an aqueous extract of
Hibiscus sabdariffa calyces on the gastrointestinal
tract. Fitoterapia Voi. 1. XII. No. 6 Pp: 475-479.
Berzynski, S.R. 1986. Anti neoplaston in cancer
therapy. History of the research drugs.
Experimental & Clinical Research, Supply 11: 1-9.
Guddum, J.H. 1955 .Polypeptides which stimulates
plain muscle. London, Livingstone. P:130.
Horton, E.W. 1959. Human Urinary Kinin Excretion.
Brit. J. Pharmacol., 14:125-132.
Kabariti, A. Mazruai, S. and Elgendi, A. 1988. Camel’s
urine: A possible anticarcinogenic agent. Arab Gulf
Journal of Science and Research Agrc.
Kitchen, L. 1984. Text Book of Experimental
Pharmacology, Isolated small intestine, 102-103.
Kroon, C.V. 1996. The Golden fountain, Autourine
therapy. Gate Way Books, ISBNO 73:2:244-256.
Martha, C. 2000. Clinically tested medicinal proved
book. Your Own Perfect Medicine.
Mona, A.K. 2003. Antibacterial effect of camel urine
(Camelus dromedaries) M.V.Sc. Faculty of Vet.
Medicine University of Khartoum, Sudan.
Mona, S. 1989. Camel urine as a hair detergent. B.Sc.
Dissertation, Ahfad University, Khartoum, Sudan.
Natalie, B. 2002. Urine Therapy (Drinking urine).
Journal of Berkeley medicine. www.ocf.berkele.
edu.
Ohaj, H.M. 1998. Clinical trial for treatment of ascitis
with camel urine M.Sc. University of the Gezira,
Sudan.
Ohaj, H.M. 1993. Clinical urine as a medicament in
Sudan. B.Sc. Dissertation, University Gezira,
Sudan.
Rang, H.P., Dale, M.M. and Ritter, J.M. 1995.
Pharmacology. 5th
(ed.) Churchill Livingstone,
London.
Rodenburg, G.L. and Nagy, S.M. 1937. Growth
stimulating and inhibiting substances in human
urine. American Journal of Cancer, 29:66.
Salwa, M.E.K. 2005. Hepatoprotective and antiparasitic
effect of female camel urine. PhD Thesis.
University of Khartoum, Sudan.
Vane, J.R. 1957. A sensitive method for the assay of 5-
HT. British Journal of Pharmacology, 12:344-349.
Wisal, G.A. 2002. Antibacterial and antifungal effect of
camel urine (Camelus dromedaries) M.V.Sc.
University of Khartoum, Sudan.

Journal of Natural Sciences Research www.iiste.org
ISSN 2224-3186 (Paper) ISSN 2225-0921 (Online)
Vol.2, No.5, 2012
9
Cytotoxicity of the Urine of Different Camel Breeds on the
Proliferation of Lung Cancer Cells, A549
Zahraa Alghamdi1*
Faten Khorshid2
1. Biology Department, Dammam University, PO box 1982, Dammam 31441, Kingdom of Saudi Arabia.
2. Biology Department, King Abdulaziz University, PO box 80216, Jeddah 21589, Kingdom of Saudi
Arabia.
* E-mail of the corresponding author: zhghamdi@yahoo.com
Abstract
Objective: Cancer is a disease characterized by uncontrolled cellular proliferation and differentiation. Nearly all
conventional cancer treatments have undesirable negative impacts, and safer chemotherapeutics would be
advantageous. Consequently, the goal of current study was to evaluate and compare the effects of urine derived
from two different camel breeds on proliferation of cultured human cancer cells. Human lung adenocarcinoma
cells (A549) were cultured in the presence or absence of varied dilutions of urine obtained from two different
camel breeds (Magateer and Majaheem). Within breeds, we compared the effects of sex and age of donor camels
on urine cytotoxicity to A549 cells. After 48 hrs, surviving A549 cells were enumerated using the
sulfarhodamine assay. A549 cell survival was lower using urine from Magateer versus Majaheem camels (84.8%
versus 94.2% of starting cell number, respectively; n=20 for both groups, p<0.001). When evaluating the effect
of camel age, urine from older Magateer camels was significantly more effective in inhibiting A549 proliferation
than was urine from younger camels of this breed. An age-related effect was not observed for Majaheem camels.
When comparing sex-effects on camel urine inhibition of A549 proliferation (n=10 in each group), we observed
a trend towards more A549 inhibition using female versus male urine, in both camel breeds; however, this
difference did not reach statistical significance. The present study confirms previous studies that showed that
camel urine can inhibit the growth of cancer cells. It also provides the first evidence that there are slight
differences in the cancer cell growth-inhibitory effect of camel urine depending on the camel breed, age, and,
possibly, sex.
Keywords: Camel breeds, Urine, Cancer cells, Cytotoxicity.
1. Introduction
Cancer is a disease characterized by uncontrolled cellular proliferation and differentiation. Nowadays, cancer is a
very common disease with a high annual incidence rate (Parkin, et al ; 1999]. Ferlay et al. (2000) reported that
worldwide more than 5 million people are diagnosed with cancer and more than 3.5 million people die from
cancer each year. Managing human malignancies still constitutes a major challenge for contemporary medicine
(Coufal et al., 2007 and Widodo et al., 2007). Although with progress in understanding cancer biology, many
new antineoplastic therapies have been developed that rely primarily on surgery, chemotherapy, radiotherapy,
hormone therapy, and immunotherapeutic approaches (Khorshid et al., 2010). However, all available therapies
are still far from ideal, in which treatment would selectively kill the malignant cells while sparing healthy tissues
and vital organ function (Grever and Charbner, 1997 and Moshref, 2007). chemotherapy resulted in an overall
increase in the survival rate and longevity of patients with life-threatening tumors, On the other hand also mean
increased exposure to toxic substances and harmful effects on different tissues ( Maino, et al.,2000).
Natural products play an important role in our healthcare system (Pezzuto, 1997 and Schwartsmann, 2000).
They offer a valuable source of potent compounds with a wide variety of biological activities and novel chemical
structures, many of which might be important for novel drug development (Vuorela, et al., 2004). Animal studies
have shown that green tea is a potent inhibitor of lung tumor development (Zhang et al., 2000). PM 701 is
another natural product readily available, cheap, and non-toxic (Khorshid, 2008). PM 701 was proven to be an
anticancer substrate (Khorshid et al., 2005, 2008, Moshref et al., 2006 and El-Shahawy et al., 2010), and was
found to be effective in limiting the metastatic spread of leukemia cells in an animal model (Moshref et al.,
2006). PM 701 is considered safe as a potential anti-cancer agent, and exerts negligible effects on vital organs
(Khorshid, 2009).
Camel urine, also a natural product, has been used traditionally in the treatment of many diseases in Arabic
countries. Drinking camel urine was shown to be effective in treating numerous cancer cases (Alhaider et al.,

Vol.2, No.5, 2012
10
2011). Moreover, according to Saudi Gazette.com, Dr. F.A. Khorshid has a potential cure for cancer based on
camel urine. After 8 years of research she has announced that nano-particles in camel urine can be used to fight
cancer. Moreover, The Saudi Center for Medical Research added that there is a tendency to start in the
production of a medical capsule containing camel’s urine for use in the treatment of cancer. In the same respect,
Alhaider et al. (2011) examined the ability of three different camel urine samples (virgin, lactating, and pregnant
sources) to modulate a well-known cancer-activating enzyme, cytochrome P 450 1a1 (Cyp 1a1) in the murine
hepatoma Hepa 1c1c7 cell line. They found that all types of camel urine, but not bovine urine, differentially
inhibited the induction of Cyp 1a1 expression by TCDD, a potent Cyp 1a1 inducer and a known carcinogen.
Virgin camel urine showed the highest degree of Cyp 1a1 inhibition, followed by lactating and pregnant camel
urine.
Khorshid (2001) stated that in vitro approaches are the best way to initially evaluate the effect of novel
biological compounds, utilizing growing mammalian cells in tissue culture. Consequently, the main goals of
current study were to: 1) evaluate the inhibitory effect of urine obtained from two different camel breeds on the
growth of lung cancer cells (A549),in vitro; and 2) study whether urine’s effect is changed according to
differences in the camel’s breed, age, or sex.
2. Materials and Methods
2.1. Study area:
The main part of this study was carried out at yebreen region located in the southern west of the eastern region at
the periphery of The Rub' alkali (Empty Quarter) included in Kingdom of Saudi Arabia.
2.2. Animals:
This study was conducted on 40 camels from two different breeds (Magateer and Majaheem). Ten males and 10
females were selected from each breed. The males ranged between 1-8 years old, whereas the females ranged
from 3 to 9 years old.
2.3. Urine sampling and storage:
Twenty milliters of urine were collected from each camel, kept in insulated boxes using freezing packs, and
transferred to the laboratory (Tissue Culture Unit, King Fahd Medical Research Center (KFMRC), King Abdul
Aziz University in Jeddah, Saudi Arabia).
2.4. Methods:
Human non-small-cell adenocarcinoma cells (A549) were obtained from the American Type Culture Collection
(ATCC) and were stored in the cell bank of tissue culture laboratory, where cytotoxicity assays were also
conducted, as pioneered by a research team working in the medical center (Khorshid et al.,2005; Khorshid and
Alameri, 2011). Different concentrations of PM 701 were used (1.0, 2.5, 5.0, 7.5, and 10 g/ml) and were
added to A549 cell monolayers. The control group of A549 cells was not treated with PM 701 and is indicated
as 0 concentration.
Cytotoxicity assays were performed using the method of Skehan et al. (1990). Cancer cells were suspended in
DMEM medium and plated in 96-well plates (104 cells/well) for 24h in a 5% CO2 incubator adjusted at 37°C
before treatment with PM701, to allow cell attachment to the bottom of the plate. Different concentrations of the
test substance (0, 1, 2.5, 5, and 10 g/ml) were then added to the cells monolayer. Triplicate wells were prepared
for each individual concentration. Cell monolayers were incubated with PM701 for 48 h at 37°C and in
atmosphere of 5% C02. After 48 h, cells were fixed using 50 µl/well trichloroacetic acid, refrigerated at 8°C for
1 hour, washed with distilled water, and then stained with Sulforhodamine B (SRB) (50 µl/well) for 30 min.
Excess stain was washed with off with acetic acid and remaining attached stain was recovered with Tris EDTA
buffer (100 µl/well). Color intensity was measured immediately in an ELISA reader at wavelength 570 nm. The
relation between surviving cells and drug concentration was plotted to get the survival curve of each cell line
after the specified period.

Vol.2, No.5, 2012
11
2.5. Statistical analysis
Statistical analysis of the data was performed with SPSS for Windows (Version 17.0.0). Data were calculated as
follows: The different urine samples were collected from the two camel breeds from both sexes. Five
concentrations of urine were tested from each individual camel (1, 2.5, 5, 7.5, 10), with 0 concentration used as
controls. Each experimental concentration was added to six tissue culture wells containing cancer cells. Forty
total urine samples were collected from each camel with their detected concentrations mentioned above, so 40
camels × 5 concentrations equals 200 urine samples. Urine specimens at the listed concentrations were directly
applied to the six wells of cultured cancer cells, so the total wells assayed equaled 1200.
3.Results and Discussion:
3.1.Differences between two camel breeds:
Data shown in Table 1 revealed that, camel urine reduced lung cancer cells to 84.75% and 92.81%, in Magateer
and Majaheem breeds, respectively, versus untreated controls (100%). Highly significant differences were
noticed between treated and control cultures when comparing urine activity within each breed and between the
different breeds (P=0.000 and 0.001, respectively). Magateer urine significantly reduced cancer cell numbers
more than did Majaheem urine.
These results are in accordance with those of Alhaider et al. (2011) who reported that drinking camel urine has
been used traditionally to treat numerous cases of cancer. The authors attributed this anticancer effect to the
ability of camel urine to modulate the well-known cancer-activating enzyme, Cyp 1a1. They found that all types
of camel urine differentially inhibited the induction of Cyp 1a1 gene expression by TCDD, the most potent Cyp
1a1 inducer and a known carcinogenic chemical. In the same respect, Eldor (1997) hypothesized that because
some cancer cell antigens are transferred through urine, through oral autourotherapy, these antigens could be
introduced to the immune system that might then create antibodies.
3.2.Camel age effects on cancer cell proliferation:
3.2.1. In the same strain:
Table 2 clarifies the effects of urine obtained from young and adult Magateer and Majaheem camels on the
growth of lung cancer cells (A549) in vitro. Urine obtained from adult Magateer camels induced a highly
significant reduction in A549 cell survival ( P≤0.004) than that obtained from the same younger breed
(81.538% versus 87.947%, respectively), while urine obtained from adult Majaheem breed induced a non-
significant (P≤ 0.179) reduction in cancer cells when compared to younger camels of the same breed (93.486%
versus 96.974%, respectively).
No available literature could be found regarding the influence of age on the anti-cancer effect of camel urine.
However, Alhaider et al. (2011) studied the ability of three different camel urines (virgin, lactating and pregnant)
to modulate the cancer-activating enzyme CyP 1a1. They found that virgin camel urine showed the highest
degree of inhibition at the activity level, followed by lactating and pregnant camel urine.
3.2.2.Age effects between the different camel breeds:
Table 3 shows a comparison between the anti-cancer effect of urine obtained from the two young camel breeds
as well as the anti-cancer effect of that obtained from the two adult camel breeds. The results revealed that urine
from young Magateer camels induced a significant (P≤0.01) reduction in the growth of cancer cells versus that
obtained from young Majaheem camels (87.947% versus 96.974%, respectively). In addition, urine obtained
from adult Magateer camels induced a significant higher reduction (P=000) of cancer cells versus that obtained
with adult Majaheem camels (81.536% versus 93.486%, respectively).
The reason for the variability in the anti-cancer efficacy of camel urine obtained from Magateer and Majaheen
breeds is not yet known. Further study is needed to determine the specific differences in the urine constituents of
each breed, to know which compound(s) is responsible for this variable effect.

Vol.2, No.5, 2012
12
3.2.3.. Sex affects camel urine-mediated cancer cell proliferation:
3.2.3.1 In the same breed:
Table 4 represents the effect of sex on the ability of camel urine to inhibit the growth of lung cancer cells in
vitro. It appears that the sex of camels within the same breed did not significantly affect camel urine-inhibition of
A549 cancer cell proliferation. However, urine of males induced a slight, though insignificant inhibition in
cancer cell proliferation versus that of females of the same breed.
3.2.3.2. In the different breeds:
Table 5 shows a comparison between the anti-cancer effect of urine obtained from males and females of the two
different camel breeds. Urine from male Magateer camels caused a significantly greater reduction in cancer cells
when compared to that induced by urine of male Majaheem camels (86.568 versus 94.014, respectively; P=.000).
Urine of female Magateer camels also induced a significantly greater reduction in cancer cells compared to that
induced by urine of female Majaheem camels (82.935 versus 91.368; P=.000). Urine from male and female
Magateer camels were more efficient in reducing lung cancer cell numbers compared with that observed using
Majaheem camel urine.
5. Conclusion
The present study confirms the findings of previous studies that camel urine can inhibit the growth of cancer
cells. It also provides the first evidence that there are differences in the cancer-inhibiting effect of camel urine
depending on the camel breed, age, and sex.
6. Acknowledgements
The authors gratefully thank King Faisal University, represented by Prof. Dr. AbdelGader Homeida and
Mr.Khalid Borsais who helped in obtaining samples. The authors also appreciate the kind help of Prof. Dr.
Hodallah Hatem, Head of the Physiology Department, Faculty of Veterinary Medicine, Cairo University, Egypt.
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Table1: Effect of camel urine obtained from Magateer and Majaheem breeds on the growth of lung cancer cells
in vitro.
Group
N
o.
Mean
%
SD Control Test Sig.
T.te
st
Sig.
Magateer
60
0
84.752 23.641 100.00 15.798
.000
*
6.15
6
.001
**
Majaheem
60
0
92.805 19.805 100.00 9.126
.000
*
. No: number of samples.
. Mean: percentage of the mean value of the number of living cancer cells.
. SD: Standard deviation
. Control: Tissue culture containing untreated cancer cells (100 cell ).
. * Comparison between the same strain treated cancer cells and non-treated cancer cells ( control).
. ** Comparison between two strains.
Table 2: Effect of urine obtained from young and adult Magateer and Majaheer breeds on the growth of lung
cancer cells (A549) in vitro.
Group No. Mean % SD T.test Sig.
Magateer
(young)
150 87.947 16.592
2.911 .004*
Magateer
(adult)
150 81.536 24.454
Majaheem
(young)
150 96.974 29.460
1.346 .179*
Majaheem
(adult)
150 93.486 11.810
. SD: Standard deviation.
. * : Comparison between young and adult at same strain.

Vol.2, No.5, 2012
15
Table 3: Comparison between the anti-cancer effect of urine obtained from the two young camel breeds as well
as the anti-cancer effect of that obtained from the two adult camel breeds.
Group No.
Mean
%
SD T.test Sig.
Magateer
(young)
150 87.947 16.592
3.499 .001*
Majaheem
(young)
150 96.974 29.460
Magateer
(adult)
150 81.536 24.454
5.476 .000*
Majaheem
(adult)
150 93.486 11.810
. * Comparison between the two strains.
Table 4: Effect of sex on the ability of camel urine to inhibit growth of lung cancer cells in vitro.
Sex No.
Mean
%
SD T.test Sig.
Male Magateer 300 86.568 15.288
1.886 .060*
Female Magateer 300 82.935 29.653
Male Majaheem 300 94.014 23.369
1.595 .111*
Female Majaheem 300 91.368 15.867
- No: number of samples.
- Mean: percentage of the mean value of the number of living cancer cells.
- SD: Standard deviation
- *Comparison between the males and females within each breed.

Vol.2, No.5, 2012
16
Table 5: In vitro comparison between the anti-cancer effects of urine obtained from females and males in the two
different camel breeds (Magateer and Majaheer).
Sex No. Mean % SD T.test Sig.
Male
Magateer
300 86.568 15.288
4.543 .000*
Male
Majaheem
300 94.014 23.369
Female Magateer 300 82.935 29.653
4.343 .000*
Female Majaheem 300 91.368 15.867
. * Comparison between the two strains.

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POSTER PRESENTATION Open Access
The effect of camel urine on islet morphology
and CCL4-induced liver cirrhosis in rat
S Al Neyadi*
, R Al Jaberi, R Hameed, J Shafarin, E Adeghate
From International Conference for Healthcare and Medical Students 2011
Dublin, Ireland. 4-5 November 2011
Introduction
Camel urine has been used for decades as a medication
for several ailments in the Middle East. Folklore medi-
cine of the Middle East has shown that, camel urine has
a beneficial effect in conditions such as liver cirrhosis.
Methods
Camel urine was given as a drink daily to normal and trea-
ted rats for 4 weeks. Glucose tolerance test was performed
at the end of the experiment. Immunohistochemistry was
used to determine the percentage distribution of insulin
and glucagon immunoreactive cells. H & E stain was used
to access liver cirrhosis in control and urine-treated rats.
Results
The administration of camel urine significantly increased
the number of insulin-positive cells in pancreatic islets.
CCL4-treated rats did not have impaired glucose toler-
ance. CCL4 caused vacuolarization of hepatic cells. Rats
treated with camel urine have improved hepatic morphol-
ogy compared to untreated controls.
Conclusions
The study shows that camel urine may contain bioactive
agents capable of preventing CCL4-induced hepatic and
pancreatic islet lesions.
Published: 9 July 2012
doi:10.1186/1753-6561-6-S4-P42
Cite this article as: Al Neyadi et al.: The effect of camel urine on islet
morphology and CCL4-induced liver cirrhosis in rat. BMC Proceedings
2012 6(Suppl 4):P42.
Submit your next manuscript to BioMed Central
and take full advantage of:
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• Thorough peer review
• No space constraints or color ﬁgure charges
• Immediate publication on acceptance
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• Research which is freely available for redistribution
Submit your manuscript at
www.biomedcentral.com/submitDepartment of Anatomy, Faculty of Medicine & Health Sciences, United Arab
Emirates
Al Neyadi et al. BMC Proceedings 2012, 6(Suppl 4):P42
http://www.biomedcentral.com/1753-6561/6/S4/P42
© 2012 Al Neyadi et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.

African Journal of Agricultural Research Vol. 5(11), pp. 1331-1337, 4 June, 2010
Available online at http://www.academicjournals.org/AJAR
DOI: 10.5897/AJAR09.686
ISSN 1991-637X © 2010 Academic Journals
Full Length Research Paper
The inhibitory effect of camel's urine on mycotoxins
and fungal growth
Amira Hassan Abdullah Al-Abdalall
Department of Botany and Microbiology, Faculty of Science for Girls, King Faisal University, El-Dammam, Kingdom of
Saudi Arabia. E -mail: Dr2000Amira@hotmail.com.
Accepted 8 January, 2010
The effect of urine and camel milk in the inhibition of biological effects of mycotoxins produced by nine
isolates of Aspergillus flavus and one isolate of Aspergillus niger isolated from pulse seeds was
studied. Where these toxins lost their ability to inhibit Bacillus subtilus growth, milk could not. Also,
our study records the effect of camel urine on mycelial growth of some roots rot fungi isolated from
seeds of pulses like Rhizoctonia solani, Fusarium moliniform, Aschocayta sp., Pythium
aphanidermatum, Sclerotinia sclerotiorum studies, also included are some storage fungi (Aspergillus
sp) isolated from coffee beans. Results proved that camel urine at low concentrations has no
significant inhibitory effect on fungal growth, while inhibition can be obviously recorded after using
high concentrations.
Key words: Camel urine, mycotoxins, mycelial growth, inhibitory effect on fungal growth.
INTRODUCTION
It is mentioned in Islam online that camel's milk and urine
have medical effects, so Islam encourages and permits
the drinking of camel milk, and camel urine is permitted in
case of necessary medical treatment (Al-Bukhhari). The
Saheeh Hadeeth says that some people came to
Madeenah and fell sick. The Prophet (peace and
blessings of Allaah be upon him) told them to drink the
milk and urine of camels, and when they drank it they
recovered and grew fat. This was narrated by Al-
Bukhaari. There are many well known health benefits,
with regard to drinking the milk and urine of camels, to
the earlier generations of medical science and they have
been proven by modern scientific researches. For
example swollen abdomen, which may indicate oedema
and liver disease (jaundice), or cancer, and thin bodies
which indicate extreme weakness, and which often
accompanies hepatitis or cancer. This may be due to the
effectiveness of camel's urine, as against all other cattle
to the active substances contained in desert plants which
benefited more of them; this was summed up by the
Prophet (peace be upon him). Many researches have
been conducted on a variety of desert plants and a strong
effect against bacteria, yeast and fungi has been found.
Kaul et al. (1976) and Zaki et al. (1984) have conducted
researches on the wormwood plant, and results have
shown strong effectiveness against bacteria, yeast and
fungi.
The chemical composition and nutritional quality of
camel milk was studied. Results showed 11.7% total
solids, 3.0% protein, 3.6% fat, 0.8% ash, 4.4% lactose,
0.13% acidity and a pH of 6.5. It contains low level of
cholesterol and sugar and is rich in the levels of Na, K,
Zn, Fe, Cu, Mn, niacin and vitamin C (Knoess, 1979).
Besides, camel milk contains low level of protein and high
concentration of insulin, and could be safely taken by
people who have high sensitivity to lactose and have
immune deficiency (Gast, 1969). Camel milk is pure white
and sugary. Camels who feed on certain diets may
produce salty milk when feed on desert weeds. There are
physiological and genetical factors affecting milk
production. Percentage of water in camel milk varies
according to the doses of water which camel drinks; it
may reach 89% in the milk if camels drink water every
day, or 91% if camels drink one hour weekly. It seems

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