Camel's Milk Protects Against Cadmium Chloride Induced Toxicity in White Albino Rats
Fahaid Al-Hashem, Mohammad Dallak, Nabil Bashir, Mohammad Abbas, Riyadh Elessa, Mohammad Khalil and Mahmoud Al-Khateeb
DOI : 10.3844/ajptsp.2009.107.117
American Journal of Pharmacology and Toxicology
Volume 4, Issue 3
Problem statement: Cadmium is one of the most dangerous occupational and environmental toxins. It is found in drinking water, atmospheric air and even in food. Cadmium is reported to be very toxic to biological systems. Until now in treating intoxication with this metal, chelating Compounds have been used, burdened with numerous undesirable symptoms. For this reason, many researches are carried out in many countries to find natural-made compounds that help in the protection against cadmium induced toxicity with fewer or no side effects. This study was conducted to demonstrate the effect of daily oral Camel's milk administration against Cadmium chloride induced toxicity in white albino rats. Approach: White albino rats of both sexes (230-250 g) were housed in standard metal cages (6 rats/cage). The experimental rats (6 in each group) distributed into two experimental groups with a shared control group received only normal saline orally (Group 1). In experimental first group a daily dose (10 mg kg1 body weight) of cadmium chloride was orally administrated to the rats for 21 days and named Cadmium chloride treated rats. In experimental second group, the same concentrations of cadmium chloride was dissolved in 2 mL of early morning fresh Camel's milk and the whole solution was administered into the experimental rats for 21 days and named Camel's milk cadmium chloride treated group. Water and food were provided ad libitum. Results: The data indicated that, in experimental Cadmium chloride treated rats, serum albumin, calcium and blood hemoglobin were decreased compared with control group received normal saline only. Moreover, Camel's milk administration with cadmium chloride showed a significant improvement of albumin, hemoglobin and calcium levels in the serum of the rats compared with cadmium chloride treated rats. Serum iron, sodium, chloride and urea levels were significantly increased in cadmium chloride treated rats compared with control group, while the addition of camel's milk to cadmium chloride decreased the high levels of these serum parameters in the treated rats. The enzyme activities of serum Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST) and serum Alkaline Phaospatase (ALP) were significantly increased by orally administration of cadmium chloride compared with control group, while adding Camel's milk to cadmium chloride decreased the high levels of these enzymes comparing with the cadmium chloride treated rats. Cadmium chloride administration resulted in a high concentration of lipid peroxidation markers; TBARS and Hydroperoxides in comparison to control group, adding camel's milk to the cadmium chloride restored the levels of these markers to their normal levels in comparing to Cadmium chloride treated rats. Also treatment with cadmium chloride alone caused a significant decrease in both the enzymatic and non-enzymatic markers of oxidative stress (superoxide dismutase and catalase) and reduced glutathione, respectively in the liver tissues of treated rats, while the administration of camel's milk with cadmium chloride increased and restored their levels to near normal in comparing with cadmium chloride treated rats. These results demonstrated that camel's milk had a protective effect against the toxicity induced by cadmium chloride. Conclusion: the above results indicated a protective effect of camel's milk oral administration against cadmium induced toxicity in white albino rats.
© 2009 Fahaid Al-Hashem, Mohammad Dallak, Nabil Bashir, Mohammad Abbas, Riyadh Elessa, Mohammad Khalil and Mahmoud Al-Khateeb. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.