Abstract
Problem statement: Nephrotoxicity is a major complication and a dose limiting factor for cisplatin therapy. Cisplatin mediated nephrotoxicity is remarkably documented by reactive oxygen species. Camel's milk has good nutritive value, antigenotoxic and anticytotoxic effects. The aim of the present study was to assess the protective effect of camel's milk against Cisplatin-induced renal oxidative stress in mice. Approach: Forty mal Swiss albino mice were randomly divided into four groups (n = 10). Group I, control group. Group II was received cisplatin (12 mg kg-1) for 5 alternate days. Group III was received camel's milk (33 mL kg-1) for consecutive 30 days. Group IV was received camel's milk (33 mL kg-1) for consecutive 30 days before administration of Cisplatin. Results: Cisplatin-induced oxidative stress was indicated by increased level of tissue Malondialdehyde (MDA), serum creatinine and urea, decreased the concentration of reduced Glutathione (GSH), Vitamin C (Vit. C) and Vitamin E (Vit. E) and decreased both activities and gene expression of Superoxid Dismutase (SOD), Catalase (CAT), Glutathione Raductase (GR) and Glutathione Peroxidase (GPx). Camel's milk reduced these biochemical changes and counteracted the deleterious effects of cisplatin Conclusion: The present study demonstrated the renoprotective potential of camel's milk against cisplatin-induced oxidative stress and renal dysfunction in mice. Hence, camel's milk has a potential to be used as therapeutic adjuvant in cisplatin nephrotoxicity.
Highlights
IntroductionMitochondria continuously scavenge Reactive Oxygen Metabolites (ROM) via the action of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, catalase and glutathione Stransferase
Preparation of kidney homogenate: The kidney was quickly removed, washed in icecold, isotonic saline and blotted on ash-free filter paper, The tissues were homogenized in 0.1 M Tris-HCl buffer, pH 7.4 using a Potter-Elvejham homogenizer at 4°C with a diluting factor of 4, the crude tissue homogenate was centrifuged at a speed of 9000 rpm for 15 min in cold centrifuge (Al-Hashem, 2009), the supernatant was kept at -20°C for estimation of Thiobarbituric Acid Reactive Substances (TBARS), reduced Glutathione (GSH), vitamin C, vitamin E Superoxide Dismutase (SOD), Catalase (CAT), Glutathione Peroxidase (GPx) and Glutathione Reductase (GR) activities
On treatment with calm’s milk, the decreased gene expression of these enzymes were brought back to near normal (Fig. 1-4), the activities of Glutathione Raductase (GR), GPx and Superoxid Dismutase (SOD) were increased significantly in camel milk treated group, but the activity of catalase enzyme was increased non significantly when compared with cisplatin group
Summary
Mitochondria continuously scavenge ROM via the action of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, catalase and glutathione Stransferase. Cisplatin is known to accumulate in mitochondria of renal epithelial cells (Santos et al, 2008). Several investigators have demonstrated that cisplatin induces ROS in renal epithelial cells primarily by decreasing the activity of antioxidant enzymes and by depleting intracellular concentrations of GSH (Huang et al, 2001). A large number of studies have accumulated documenting the beneficial effects of a variety of antioxidants in cisplatininduced nephrotoxicity. Agents such as superoxide dismutase, dimethylthiourea and GSH have been shown to reduce the degree of renal failure and tubular cell damage when administered simultaneously with cisplatin in rats (Tsuji et al, 2009)
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