Spermatogenesis disorder and activation of BCL2/Bax apoptosis pathway in the rat testis after co-exposure to PM2.5 and gaseous pollutants: A ‎possible interaction with GATA4 and GATA6

Abstract

Abstract The exposure of men to particulate matter and gaseous air pollution can ‎seriously threaten spermatogenesis. However, its specific molecular ‎mechanism is a mystery. This in-vivo rat model study has focused on the effect of coexposure to ambient fine particulate matter (PM2.5) plus gaseous pollutants on the oxidant/antioxidant system in the testis and its role in the changes of sex hormones, spermatogenesis, activation of apoptosis BCL2/BAX signaling pathway and GATA4 and GATA4 protein expression in the testis cells. Twenty-one male Wistar albino rats were ‎randomly divided into three groups including the control group (air with the standard condition) and the GAS (gaseous pollutants alone) and Gas + PM2.5 (PM2.5 plus gaseous pollutants) groups exposed for 3 months (4 days a week, 5 h a day). The results revealed that coexposure to gaseous pollutants and PM2.5 significantly decreased sperm motility, sperm count, and the Johnson score, and increased sperm mortality and sperm DNA fragmentation. Also, in the Gas + PM2.5 group, the levels of testosterone and FSH in serum and the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) in the testis significantly decreased, while the level of malondialdehyde (MDA) increased compared to the control group. The expression of BCL2, GATA4, and GATA6 proteins in the testis significantly decreased in the Gas + PM2.5 group, while Bax protein expression increased compared to the control group. Altogether, coexposure to ambient PM2.5 plus gaseous pollutants could induce oxidative stress in the testis and decrease hormone secretion and apoptosis in sperms via activating BCL2/BAX pathway and possible crosstalk with GATA 4 and GATA 6 proteins.