Table 1.

Data extraction table.

Author	Subject (n)	Dosage	Type of camel	Methodology		Results	Conclusion
				Treatment Group	Measurement
(Al-Harbi et al., 1996)	Mice (60)	Camel urine (CU) with a 5%–100% concentration as daily drinking water for 7 days. Average of 5.4–5.82 ml camel urine per mouse.	Male camel (Camelus dromedarius) from Riyadh, Saudi Arabia	All animals were divided into 12 groups (5 mice per group). Each group was treated with; 1)tap water (control) 2)cyclophosphamide (CP) (100 mg/kg) 3)5% CU 4)15% CU 5)25% CU 6)50% CU 7)100% 8)pretreatment with 5% CU followed by 100 mg/kg CP 9)pretreatment with 15% CU followed by 100 mg/kg CP 10)pretreatment with 25% CU followed by 100 mg/kg CP 11)pretreatment with 50% CU followed by 100 mg/kg CP 12)pretreatment with 100% CU followed by 100 mg/kg CP	1.Micronucleus test 2.Estimation of protein and nucleic acid 3.Malondialdehyde (MDA) concentration 4.Glutathione level	1) Micronucleus test: •CU failed to induce any significant effects on the frequency of micronucleated polychromatic erythrocytes (PCE) in femoral cells compared with control. •Significant decrease in the number of PCE compared with normochromic erythrocytes (NCE). •Significant decrease in PCE/NCE ratio in groups 4, 5, 6 and 7 •Group 2 significantly increased the incidence of micronucleated PCE and decreased PCE/NCE ratio. •Pretreatment with CU failed to alter the effect of CP on the incidence of micronucleated PCE and PCE/NCE ratio but significantly increased NCE in groups 11 and 12. 2) Estimation of protein and nucleic acid: •Significant reduction in DNA and RNA levels in hepatic cells in groups 6 and 7 compared with control, but no effect on protein level. •Pretreatment with CU significantly elevated CP-induced DNA inhibition (groups 11 and 12), RNA (groups 9, 10, 11 and 12) and protein contents (groups 10, 11 and 12). 3) MDA concentration: •Groups 5, 6 and 7 showed a significant increase in MDA. •Pretreatment with CU (groups 10, 11 and 12) further increased MDA level. 4) Glutathione level: •Glutathione levels significantly reduced in groups 4, 5, 6 and 7. •Pretreatment with CU (groups 10, 11 and 12) further decreased glutathione level.	CU shows cytotoxic activity and non-clastogenic nature in mice induced with CP.
(Mahmoud et al., 2019)	Adult male Sprague Dawley rats (30)	2 ml/100 g by oral intubation for 60 days	Female lactating camel from Egypt	All animals were divided into three groups (10 rats per group). Each group was treated with: 1)normal water (control) 2)CCl4 (3 ml/kg) for 1 day 3)CCl4 (3 ml/kg) for 1 day and CU (2 ml/100 g) for 60 days	1)In vitro assessment of CU antioxidant activity 2)Serum biochemical analysis 3)Histopathological examination	1. In vitro assessment of CU antioxidant activity: •CU (100 µg) showed strong free radical scavenging activity against SOR, H2O2 and FRAP free radicals (p = 0.001). 2. Serum biochemical analysis: •CU significantly decreased in SGPT and SGOT and increased in serum albumin in CCl4 intoxicated rats. 3. Histopathological examination: •Hepatic tissue shows significant improvement with no lytic necrosis or portal inflammation and less marked fibrous tissue expansion in rats treated with CCl4 and CU.	CU shows a protective and curative role against hepatic dysfunction via antioxidative, anti-free radical scavenging activities of its present volatile metabolites and essential inorganic elements.
(Al-Yousef et al., 2012)	Human cancer cell line: MCF 10A, MDA-MB-231, U2OS, DAOY, LoVo, HCT-116, MED-1, MED-8, MED-13 and HFSN1	16 mg/ml was added to every cell line	Young female camel (Camelus dromedaries)	All cell lines were divided into two groups (control and treatment). Control groups were not treated, and treatment groups received 16 mg/ml CU. For PBMC cytotoxicity test, cells were treated with different concentrations of CU for 3 days.	1.Cytotoxicity test 2.Apoptosis 3.Cell proliferation analysis 4.Cancer-related genes 5.Cytotoxic test on PBMCs	1. Cytotoxicity test: •More than 80% of MDA-MB-231 cells (breast cancer cells) died in response to 16 mg/ml CU but had no effect on MCF 10A cells (non-tumorigenic breast epithelial cells) with the same concentration. •Cells were divided into two groups: (1) CU-resistant cells included MCF 10A, HFSN-1, U2OS, MCF-7, MED-8, LoVo and HCT-116 and (2) CU-sensitive cells, with more than 50% cell death, including MDA-MB-231, DAOY, MED-4 and MED-13. 2. Apoptosis: •CU treatment for 72 h triggered apoptosis (90%) with only a slight necrosis proportion. •DAOY and MED-4 showed high sensitivity, whilst MED-3 showed clear resistance. 3. Cell proliferation analysis: •CU triggered a decrease in anti-apoptotic protein Bcl-2 and an increase in pro-apoptotic protein Bax. •CU decreased the expression of the anti-apoptotic survivin protein. 4. Cancer-related genes: •Addition of CU immediately stopped MDA-MB-231 cell proliferation. •CU down-regulated β-catenin, cyclin D1 and survivin and up-regulated cyclin-dependent kinase inhibitor p21. 5. Cytotoxic test on PBMCs: •CU triggered apoptosis in MDA-MB-231 cells. •CU (20 mg/ml) increased the level of CD3 + CD9 + and CD3 + HLA-DR + . •CU stimulated the production of IFN-ɣ and reduced IL-6, IL-4 and IL-10.	Camel urine has anticancer effects on the various human cancer cell lines.
(Alhaider et al., 2011)	Hepa 1c1c7 cell line	Camel urine (CU) 15 µl/ml added to Hepa 1c1c7 cell line	Female virgin, prenant and lactating camel (Camelus dromadaries)	Hepa 1c1c7 cells were preincubated with either CU or BU (15 µl/ml) before incubation with 1 nM TCDD	1.MTT assay 2.TCDD-induced Cyp1a1 catalytic activity 3.Cyp1a1 mRNA level 4.Cyp1a1 protein expression 5.Inhibition of AhR transformation and XRE binding 6.Inhibition of AhR-dependent reporter gene expression	1)MTT assay: •Neither CU nor BU was toxic to Hepa 1c1c7 cells up to 15 µl/ml. •Cell viability decreased by 35% in pregnant CU (50 µl/ml); 12% and 15% at 25 µl/ml and 50 µl/ml, respectively, in virgin BU; 15 µl/ml of both CU and BU were chosen in the subsequent tests. 2)TCDD-induced Cyp1a1 catalytic activity: •Virgin CU showed the highest inhibitory effect (80%), followed by lactating CU (70%) and pregnant CU (54%). •The obtained inhibition was similar to that of resveratrol (25 µM, positive control), which inhibited 50% of TCDD-induced Cyp1a1 catalytic activity. •Virgin CU significantly inhibited 45% of TCDD-induced Cyp1a1 mRNA. •Resveratrol (25 µM) significantly inhibited TCDD-induced Cyp1a1 mRNA by 20%. 3)Cyp1a1 protein expression: •Virgin and lactating CU caused significant TCDD-induced Cyp1a1 protein level inhibition by 65% and 45%, respectively. 4)Inhibition of AhR transformation and XRE binding: •Virgin CU significantly inhibited the TCDD-induced activation of AhR and transformed the AhR/ARNT/XRE complex. 5)Inhibition of AhR-dependent reporter gene expression: •Virgin CU caused a significant inhibition of the TCDD-induced AhR-dependent reporter gene expression.	Camel urine inhibits the TCDD-mediated effect, at least in part by inhibiting the expression of Cyp1a1, a cancer-activating gene, at both the transcriptional and the post-translational levels through an AhR-dependent mechanism.
(Hu et al., 2017)	Sprague–Dawley rats (95)	5 ml/kg of camel milk (CM) and urine (CU) were given orally	Camel from Hargeisa, Somaliland	All animals (5 rats per group) were treated with saline (5 ml/kg), cimetidine (100 mg/kg), CM (5 ml/kg) or CU (5 ml/kg) and induced with any one of the ulcer agents (HCl/EtOH (0.2 ml/animal), indomethacin (50 mg/kg) or water restraint stress-induced ulcer (3 h))	1)Acute toxicity study 2)Ulcer index (UI) 3)Ulcer inhibition degree	1)Acute toxicity study: •Administration of CM and CU at a high dosage of 10 mg/kg did not show any signs of toxicity and mortality during two weeks of observation. 2)HCl/EtOH-induced ulcer: •Administration of cimetidine, CU, and CM showed significant (p < 0.05) ulcer inhibition of 83.07%, 60.5% and 100%, respectively. •The mean UI was reduced significantly (p < 0.05) from 17.2 ± 0.84 mm in the negative control group to 2.8 ± 0.84, 6.8 ± 0.84, and 0 ± 0.00 mm in the cimetidine, CM and CU groups, respectively. 3)Indomethacin-induced ulcer: •Administration of cimetidine, CM and CU reduced the formation of hemorrhagic spots by 100%, 33.3% (UI = 2.0 ± 0.0) and 66.7% (UI = 1.0 ± 0.0), respectively. •No ulcer could be seen in the CM and CU groups, both exerting a 100% healing effect. The cimetidine group showed a lesion area (3.0 ± 0.71 mm) with a significant healing effect of 60.5%. 4)WRS-induced ulcer: •Administration of cimetidine and CU showed 100% ulcer inhibition, whilst CM inhibited ulcer formation by 50%.	Administration of CM and CU may have strengthened the mucosal barrier against endogenous and exogenous ulcerogenic agents in HCl/EtOH, non-steroidal anti-inflammatory drugs and WRS-induced gastric damage. CM and CU also showed a strong ulcer-healing effect in indomethacin-induced gastric damage.
(Alhaidar et al., 2011)	Healthy human volunteers	0.05 ml CU was added to human platelet-rich plasma (PRP)	Female virgin, pregnant and lactating domesticated camels (Camelus dromedaries)	0.05 ml of CU was added to human PRP before 0.05 ml of ADP or AA (aggregating agent) was added	Platelet inhibitory activity, aggregation responses to adenosine diphosphate (ADP) and arachidonic Acid (AA), PFA-100 closure time	•Virgin, pregnant and lactating CU significantly inhibited aggregation response to ADP and AA (p < 0.001). •Lactating CU showed the most potent platelet inhibitory activity against ADP- and AA-induced aggregation (p < 0.001). •CU also prolonged PFA-100 closure time.	CU showed antiplatelet actions and provided an essential foundation of scientific evidence to explore CU as a therapeutic antiplatelet agent.