Infertility in male wistar rats induced by cadmium chloride: Role of ascorbic acid

Objective: Cadmium is a highly toxic and carcinogenic environmental contaminant. Exposures to cadmium have been reported to reduce male fertility and there are several hypotheses that suggest how reduced male fertility may result from incorporation of cadmium. The purpose of this study was to determine the role of testicular ascorbic acid level in cadmium mediated oxidative damage on rat testis. Methods: Adult male wistar rats (n=6/group) were divided into three groups, one control group and two experimental groups ( low dose and high dose). The experimental groups were injected with single dose of 1 mg/kg BW cadmium chloride in low dose group and with 2 mg/kg BW cadmium chloride in high dose group, intraperitoneally respectively. The control group received the same volume of 0.9% saline intraperitoneally. Animals were sacrificed 15 days after cadmium chloride or saline injection. The epididymal sperm count, sperm abnormalities, testicular weight, tissue level of lipid peroxidation and testicular ascorbic acid levels were estimated. Results: Exposure of rats to different doses of cadmium showed a decrease in the testicular weight (P<0.001) and, sperm count (P<0.001), ascorbic acid level (P<0.001), and increase in the testicular level of lipid peroxidation and in the incidence of abnormal sperms (P<0.001). Exposure to high dose of cadmium showed a significant decrease in testicular weight (P<0.001) and sperm count and increase in lipid peroxidation compared to low dose group. Ascorbic acid level decreased significantly in high dose group compared to low dose group. Conclusion: Therefore, the present study suggests that cadmium has deleterious effect on spermatogenesis and one of the possible mechanism in cadmium induced oxidative damage on rat testis cell might be mediated through its effect on reducing ascorbic acid level.