Cardiopreventive effects of camel milk against carbon tetrachloride induced oxidative stress, biochemical and histological alterations in mice.

The present study was designed to examine the preventive effects of camel milk (CM) against the toxic effects of acute exposure to carbon tetrachloride (CCl4) on the heart tissue of mice. Administration of a single dose of CCl4 caused cardio toxicity as monitored by an increase in lipid peroxidation (thiobarbituric acid reactive substances), protein carbonyl level and antioxidant markers (superoxide dismutase, catalase, glutathione peroxidase, glutathione and vitamin C) in the heart tissue. Moreover, CCl4 caused a distinguished rise of plasma aspartate aminotransferase, lactate dehydrogenase, troponin I, and creatine kinase activities. Furthermore, CM ameliorated biochemical and histological parameters as compared to CCl4-treated group. Overall, this study indicates that CM is efficient in inhibiting oxidative stress induced by CCl4 and suggests that the administration of this milk may be helpful in the prevention of cardio-toxicity complications.