Abstract

Objective: This study was designed to investigate the effects of melatonin as an antioxidant, in prevention and treatment of cadmium (Cd)-induced renal toxicity in rats.

Materials and methods: Fifty adult male Sprague-Dawley rats weighing 340 to 370 g were used. Renal toxicity was induced with the use of 200 µg/ml of cadmium chloride in tap water. Ten rats were assigned to receive only tap water as the control group for three months and seven days. Two study groups were designed. To investigate the ability of melatonin to prevent Cd damage (Study 1), 10 rats received Cd and 10 rats received Cd plus 0.02% co-treatment melatonin in tap water for three months. To test whether melatonin would reverse CD-induced damage to the kidney (Study 2), 10 rats received Cd in tap water for three months+7 days, and 10 rats received Cd for three months followed by administration of high-dose (0.08%) melatonin in tap water for seven days.

Results: Cadmium exposure significantly increased the kidney malondialdehyde (MDA) levels, as a marker of lipid peroxidation, decreased the kidney superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities, increased Cd concentrations in the renal cortex, but did not change glomerular filtration rate (GFR) and fractional excretion of sodium (FE-Na). In Study 1, melatonin decreased MDA levels, increased SOD, CAT and GSH-Px activities. In Study 2, melatonin decreased the kidney MDA levels, increased the SOD activity, but did not change the CAT and GSH-Px activities. Kidney accumulation of Cd did not change in both melatonin-treated groups. Histopathologically, Cd intake affected proximal tubules of the nephron more than the glomerular parts. Melatonin did not change these alterations.

Conclusion: Our findings suggest that Cd-induced renal toxicity is related with oxidative stress and exogenously administrated melatonin might reduce the toxic effects of Cd on kidney without any reduction in tissue Cd burden.