Camel's Milk Protects against Aluminum Chloride-Induced Toxicity in the Liver and Kidney of White Albino Rats

Abstract

Problem statement: Aluminum chloride (AlCl₃) is commonly used in daily life but it can be potentially toxic. Therefore, the present study was carried out to investigate the protective effects of camel’s milk against aluminum-induced biochemical alterations and oxidative stress in the liver and kidney of white albino rats. Approach: White albino male rats (230-250 g) were divided into three groups of 10 rats: a control group treated with normal saline, the AlCl₃-treated group and the camel’s milk-AlCl₃-treated group. The AlCl₃ treated group received 0.5 mg kg^-1 of AlCl₃ orally. The camel’s milk-AlCl₃-treated group was fed 1 mL of fresh camel’s milk 10 minutes prior to the administration of oral AlCl₃. All rats were treated every day for 30 days. Liver and kidney biochemical serum parameters were analyzed. Lipid peroxidation, as determined by the tissue concentrations of thiobarbituric acid reactive substances (TBARS) and hydrogen peroxide (HP), and the oxidative stress status, as measured by glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) activity, were evaluated in the kidney and liver of treated rats. Results: Data showed that the oral administration of AlCl₃ resulted in statistically significant increases in the serum levels of urea, creatinine, bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), cholesterol and triglycerides; the total amount of protein and albumin were also significantly decreased. However, these parameters were within normal levels in the rats given camel’s milk prior to AlCl₃. Additionally, oral administration of AlCl₃ induced lipid peroxidation in the liver and kidney, which was indicated by a significant increase in lipid peroxidation biomarkers (TBARS and HP) and a significant decrease in the activities of GSH, SOD and CAT. In all rats treated with camel’s milk before being given AlCl₃, lipid peroxidation and oxidative stress parameters were within normal levels. Conclusion: Treatment with camel’s milk prior to AlCl₃ exposure alleviates AlCl₃-associated hazards and protects the kidney and liver from AlCl₃ toxicity.