Human black and white-skinned races exhibited differences in platelet aggregation. However, no similar differences were described on white and black camels. This study aims to find out whether black and white camel skin color is associated with differences in camel platelet aggregation responses or the platelet inhibitory activity of their urine. Platelet aggregometry was undertaken in black and white camels, in response to adenosine diphosphate (ADP), Arachidonic acid (AA), Epinephrine (EPN), collagen, and Ristocetin. Platelet aggregometry was also done in human PRP after the addition of raw and serially diluted (1:2, 1:4 and 1:8) white and black camel urines. In black camels, platelet aggregation in response to ADP, AA, EPN and Collagen were slightly higher than in white camels. The addition of raw camel urine collected from mixed population of black and white camels to human platelets resulted in inhibition of platelet aggregation. Serial dilutions of camel urine (1:2, 1:4, 1:8) resulted initially in loss of the inhibitory action followed by enhancement of human platelet aggregation responses to ADP and AA. The neat and serially diluted white camel urines caused more inhibition of the human platelet aggregation responses than the black camel urines. This study uncovered a new biological feature in the camels. The camel skin color seems to be associated with different platelet aggregation responses as well as different antiplatelet activity of the camel urine; white camel urine was found to cause more platelet inhibition than black camel urine.

Methotrexate (MTX) is widely used chemotherapeutic and immune suppressant agent. Hepatotoxicity is a common side effect of chronic MTX therapy. This study investigated the hepatoprotective properties of camel milk (CM) and camel urine (CU) in hepatotoxicity induced by intraperitoneal injection of MTX 20 mg/kg. The MTX-intoxicated animals showed elevated serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, fasting blood glucose (FBG), liver DNA fragmentation marker (DFF-40), and serum and liver cytokeratin (CK-18), decreased serum proteins, albumin, fibrinogen, and total antioxidant capacity (TAC). Decreased antithrombin (AT) was associated with prolonged prothrombin time (PT) and activated partial thromboplastin time (APTT). Treatment with CM and CU for four weeks decreased the liver enzymes, FBG, DFF-40, and CK-18 levels and increased total proteins, albumin, fibrinogen, and TAC. However, the changes in AT, PT, and APTT persisted. CM and CU showed promising abilities to counteract MTX hepatotoxicity and they exerted cytoprotective, antiapoptotic, antioxidative, antihyperglycemic, and antithrombotic effects.

Background: Numerous medical properties have been attributed to camel urine (CU), including anticancer activity as reported in the literature. Laboratory studies have also demonstrated that CU inhibits platelet aggregation in a manner similar to aspirin (acetylsalicylic acid, ASP), a well-known antiplatelet agent with documented anticancer relevance. It is therefore of interest to further explore similarities in the actions of these agents using molecular approaches. This study aimed to characterize the effect of CU on the expression of human platelet GP receptors (CD41, CD61, CD42a, and CD42b) and to compare these effects with those of aspirin, a well-established antiplatelet agent. Methods: The effect of CU on human platelet aggregation in response to adenosine diphosphate (ADP) and arachidonic acid was evaluated using light transmission aggregometry. CU that showed an inhibitory effect on platelet aggregation was subsequently used for flow cytometric analysis, and ASP was used for comparison as a positive control. Platelet rich plasma was prepared from human blood, and washed platelets were subsequently isolated. The washed platelets were incubated with fresh CU (9.1% v/v; n = 8) or ASP (stock concentration: 81 mg/mL n = 6) for 5 min at room temperature, while parallel untreated samples served as controls. Platelet GP receptor expression was subsequently evaluated by flow cytometric quantification of CD61, CD41, CD42a, and CD42b using a BD FACSCalibur and BD FACSCanto II. Results: Flow cytometric analysis revealed that both CU and ASP caused a significant reduction in the expression of CD61, CD41, CD42a, CD42b, and the CD41/CD61 complex compared with untreated samples. However, ASP exhibited a stronger inhibitory effect than CU. ASP induced greater inhibition of CD41 (48.3%) followed by CD61 (41.5%), whereas CU resulted in 1: 30.6% and 28.2% inhibition of CD61 and CD41, respectively. Conclusion: These findings indicate that CU possesses antiplatelet activity, which may warrant further investigation as a potential contributor to its reported anticancer effects.