Lead aggravates the diabetic-induced reproductive toxicity in male Wistar rats.

Abstract

Diabetes, an unresolved metabolic disorder, and lead contamination are prevalent problems in contemporary society. Previously, we have reported that either diabetes or lead exposure resulted in reproductive toxicity in male Wistar rats. The aim of this study was to evaluate whether diabetic rats exposed to lead demonstrate a higher degree of reproductive toxicity when compared with lead-exposed control rats. Diabetes was induced by injecting a single dose of streptozotocin (50 mg per kg body weight). Control and diabetic rats were exposed to lead at a concentration of 819 mg L-1 (0.15% lead acetate) through drinking water for a period of 30 days and assessed for reproductive and oxidative end points. The relative weights of the testes, epididymis, seminal vesicles, and the prostate gland were significantly decreased in diabetic rats. Daily sperm production, epididymal sperm count, motile, viable and HOS-tail swelled sperms, serum testosterone levels and testicular 3β- and 17β-hydroxysteroid dehydrogenase activity levels were significantly decreased in diabetic rats. Significant reductions in testicular and epididymal antioxidant enzyme activity levels and glutathione levels were observed in diabetic rats with an elevation in the levels of superoxide anions, hydrogen peroxides, and lipid peroxidation. A significant reduction in the number of implantations associated with elevated pre- and post-implantation losses was observed in females mated with diabetic males. Mild histopathological malformations were observed in the testis of the diabetic rats. Similar reproductive and oxidative toxicities were observed in lead-exposed control rats. Furthermore, lead exposed diabetic rats showed additional deterioration in reproductive end points and a noteworthy elevation in oxidative toxicity, suggesting that treatment with lead exacerbates reproductive toxicity in streptozotocin-induced diabetic rats.