2009American Journal of Applied SciencesRequires access

Camel’s Milk Alleviates Oxidative Stress and Lipid Peroxidation Induced by Chronic Aluminum Chloride Exposure in Rat’s Testes

Fahaid Al‐Hashem

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Abstract

Problem statement: The present study was carried out to examine the effectiveness of Camel’s milk in alleviating aluminum chloride (AlCl3)-induced oxidative stress and lipid peroxidation in rat testes. Approach: White albino male rats (230-250 g) were divided into three groups of 10 rats: A control group, treated with normal saline and two experimental groups, the AlCl3 treated group and the Camel’s milk-AlCl3 treated group. The first experimental group, the AlCl3 treated group, received 0.5 mg kg−1 of AlCl3 orally. The second experimental group was fed 1 mL of fresh Camel’s milk 10 min prior to the administration of oral AlCl3. All rats were treated every day for 30 days. Lipid peroxidation, as determined by testicular concentration of Thiobarbituric Acid Reactive Substances (TBARS) and Hydroperoxide (HP) levels and the oxidative stress status, as measured by glutathione (GSH) levels, Superoxide Dismutase (SOD) and Catalase (CAT) activity, were evaluated in the rat testes. Results: Oral administration of AlCl3 induced lipid peroxidation and oxidative stress in rat testes, which was indicated by a significant increase in lipid peroxidation biomarkers (TBARS and HP) and a significant decrease in the GSH content and SOD and CAT activities. When rats received Camel’s milk before being given AlCl3, lipid peroxidation and oxidative stress parameters were restored to normal levels. In the testes from rats fed Camel’s milk TBARS and HP levels were significantly reduced and, conversely, GSH content, SOD and CAT activities were significantly increased compared to rats that received only AlCl3. Conclusion: Treatment with Camel’s milk prior to AlCl3 alleviates AlCl3-associated hazards and protects testicular tissue from AlCl3 toxicity.

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Problem statement: The present study was carried out to examine the effectiveness of Camel’s milk in alleviating aluminum chloride (AlCl3)-induced oxidative stress and lipid peroxidation in rat testes. Approach: White albino male rats (230-250 g) were divided into three groups of 10 rats: A control group, treated with normal saline and two experimental groups, the AlCl3 treated group and the Camel’s milk-AlCl3 treated group. The first experimental group, the AlCl3 treated group, received 0.5 mg kg−1 of AlCl3 orally. The second experimental group was fed 1 mL of fresh Camel’s milk 10 min prior to the administration of oral AlCl3. All rats were treated every day for 30 days. Lipid peroxidation, as determined by testicular concentration of Thiobarbituric Acid Reactive Substances (TBARS) and Hydroperoxide (HP) levels and the oxidative stress status, as measured by glutathione (GSH) levels, Superoxide Dismutase (SOD) and Catalase (CAT) activity, were evaluated in the rat testes. Results: Oral administration of AlCl3 induced lipid peroxidation and oxidative stress in rat testes, which was indicated by a significant increase in lipid peroxidation biomarkers (TBARS and HP) and a significant decrease in the GSH content and SOD and CAT activities. When rats received Camel’s milk before being given AlCl3, lipid peroxidation and oxidative stress parameters were restored to normal levels. In the testes from rats fed Camel’s milk TBARS and HP levels were significantly reduced and, conversely, GSH content, SOD and CAT activities were significantly increased compared to rats that received only AlCl3. Conclusion: Treatment with Camel’s milk prior to AlCl3 alleviates AlCl3-associated hazards and protects testicular tissue from AlCl3 toxicity.

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Available abstract

Problem statement: The present study was carried out to examine the effectiveness of Camel’s milk in alleviating aluminum chloride (AlCl3)-induced oxidative stress and lipid peroxidation in rat testes. Approach: White albino male rats (230-250 g) were divided into three groups of 10 rats: A control group, treated with normal saline and two experimental groups, the AlCl3 treated group and the Camel’s milk-AlCl3 treated group. The first experimental group, the AlCl3 treated group, received 0.5 mg kg−1 of AlCl3 orally. The second experimental group was fed 1 mL of fresh Camel’s milk 10 min prior to the administration of oral AlCl3. All rats were treated every day for 30 days. Lipid peroxidation, as determined by testicular concentration of Thiobarbituric Acid Reactive Substances (TBARS) and Hydroperoxide (HP) levels and the oxidative stress status, as measured by glutathione (GSH) levels, Superoxide Dismutase (SOD) and Catalase (CAT) activity, were evaluated in the rat testes. Results: Oral administration of AlCl3 induced lipid peroxidation and oxidative stress in rat testes, which was indicated by a significant increase in lipid peroxidation biomarkers (TBARS and HP) and a significant decrease in the GSH content and SOD and CAT activities. When rats received Camel’s milk before being given AlCl3, lipid peroxidation and oxidative stress parameters were restored to normal levels. In the testes from rats fed Camel’s milk TBARS and HP levels were significantly reduced and, conversely, GSH content, SOD and CAT activities were significantly increased compared to rats that received only AlCl3. Conclusion: Treatment with Camel’s milk prior to AlCl3 alleviates AlCl3-associated hazards and protects testicular tissue from AlCl3 toxicity.

Key concepts: Oxidative stress, Lipid peroxidation, Oxidative damage, Chemistry, Chloride, Biochemistry, Endocrinology, Biology

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