Increase in the expression of inducible nitric oxide synthase on exposure to bisphenol A: A possible cause for decline in steroidogenesis in male mice

• BPA induces oxidative stress in the testicular tissues of male mice.
• BPA increases the iNOS expression in mice testis leading to impaired steroidogenesis.
• An increase in iNOS expression adversely affects the StAR expression.
• Lower doses of BPA are found to be more toxic to the male spermatogenic process.

Bisphenol A (BPA) is a well-known plasticizer and xenoestrogen that is responsible for many acquired reproductive difficulties, especially in men. Despite the prevalence of BPA in society, the mechanism behind reproductive deficits remains elusive. The present study investigates the mode of BPA's action by evaluating its effect on the expression of inducible nitric oxide synthase (iNOS) and steriodogenic acute regulatoryprotein (StAR) in male mice testis. Swiss albino mice were treated with a range BPA concentrations of 0.5, 50 and 100 μg/kg body weight/day intraperitoneally for 60 days. Several markers of oxidative stress and male fertility were investigated. Nitrite levels, malondialdehyde levels and testicular injury scores were elevated whereas the sperm count, serum testosterone levels and catalase activity were reduced in the BPA groups. Mechanistically, an increase in iNOS expression was observed in the testis whereas the expression of the StAR was down regulated in the BPA treated mouse. These results suggest that BPA induces oxidative stress by altering the expression of iNOS, which consequently leads to the down regulation of StAR expression in the testis of male mouse.