Protective effect of indomethacin on vanadium-induced adrenocortical and testicular damages in rat

Abstract

Vanadium toxicity is a globally recognized threat to the reproductive health of man and animal. However the mechanism of vanadium-induced damage to the testicular and adrenocortical tissues is not fully characterized. It was hypothesized that prostaglandins may partially mediate the inflammatory response to vanadate damage. In this study prostaglandin (PG) mediated effects of vanadate on testicular and adrenocortical functions was substantiated by using indomethacin to block prostaglandin synthesis. Significant inhibition of spermatogenesis, decreased serum level of testosterone and gonadotropins in the vanadium-exposed group of rats indicated the damaging effects of vanadium-induced reactive oxygen species. This was also reflected in the appreciable increase in testicular lipid peroxidation (LPO) level and decline in the activities of steroidogenic and antioxidant enzymes. Histopathological studies revealed regressive and degenerative changes in testis. However, inhibition of cyclooxygenase activity by indomethacin increased steroid hormone production, gonadotropin level, elevated the specific activities of enzymes and decreased LPO level in rat testis exposed to vanadium. Vanadium also caused prostaglandin mediated adrenocortical hyperactivity, as inhibition of PG synthesis abolished these adrenal responses to vanadium. The studies showed that vanadium toxicity is directly linked to stimulation of prostaglandin synthesis. Therefore, indomethacin can be a good prospect to alleviate vanadium induced male infertility.