Selenium attenuates bisphenol A incurred damage and apoptosis in mice testes by regulating mitogen-activated protein kinase signalling.

Being a vital micronutrient, along with a trace element, selenium (Se) protects the cells from oxidative stress (OS) in the form of selenoproteins. Bisphenol A (BPA) is a xeno-oestrogenic compound that adversely affects the spermatogenesis process by inducing oxidative stress, which ultimately leads to male infertility. Therefore, it is hypothesised that Se could protect against BPA-induced OS, and further germ cell death by modifying mitogen-activated protein kinase (MAPK) signalling. Male Balb/c mice were divided into four groups: Group I (C) (0.2 ppm Se), Group II (Se) (0.5 ppm Se), Group III (BPA) (0.2 ppm Se, and BPA = 1 mg/kg orally) and Group IV (Se + BPA) (0.5 ppm Se, and BPA = 1 mg/kg bodyweight orally). Results indicated that BPA-treated animals demonstrated a marked decrease in antioxidant enzyme activities (superoxide dismutase, catalase, redox ratio), a marked elevation in the expressions of stress-activated kinases (c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and p38) and the expressions of pro-apoptotic markers (caspase-9, caspase-8 and caspase-3). However, Se supplementation considerably restored the antioxidant enzyme activities and lowered the expressions of stress-activated kinases, which further down-regulated the apoptosis. Thus, Se supplementation demonstrated to be effective against BPA provoked testicular damage.