Vanadium-Induced Testicular Toxicity and Its Prevention by Oral Supplementation of Zinc Sulphate

Abstract

ABSTRACTTransition metal vanadium has been shown to modulate the cellular redox potential and catalyze the generation of reactive oxygen intermediates. Since free radical production and lipid peroxidation are potentially important mediators in testicular physiology and pathophysiology, the present study was conducted to elucidate the vanadium-induced oxidative damages in rat testis and the ameliorative role of zinc sulphate against such adverse effects of vanadium. Adult male rats were dosed for 26 days with daily intraperitoneal injection of 0.4 mg V/kg body weight as sodium metavanadate. One group of rats was treated with zinc sulphate orally simultaneously with vanadium for 26 days, while the other group was treated with zinc sulphate alone. Changes in testicular and accessory sex organ weight, different varieties of germ cells at stage VII of spermatogenic cycle, epididymal sperm count, and enzymatic (Δ53β- HSD, 17β- HSD, SOD, catalase), lipid peroxidation, and hormonal milieu were monitored. Vanadium treatment resulted in a significant increase in the testicular lipid peroxidation and caused a marked inhibition in the activities of antioxidant and steroidogenic enzymes. Histopathological examination revealed inhibition of spermatogenesis and the preferential loss of maturing and elongated spermatids. However, coadministration of zinc sulphate to vanadium-treated animals resulted in normalizing these parameters appreciably, emphasizing the therapeutic potentials of zinc. Taken together, the results suggest that an increase in free radical formation relative to loss of the antioxidant defense system during vanadium exposure may render testis more susceptible to oxidative damage, leading to their functional inactivation. However, zinc sulphate supplementation can be an effective antidote in the treatment of vanadium poisoning.