Spermatogenesis, a highly coordinated process, is prone to environmental insults which may lead to impaired spermatogenesis or, at worst, infertility. Bisphenol A (BPA) is a well-known global environmental toxicant and a ubiquitous oestrogenic chemical. This study evaluated the role of selenium (0.5 ppm sodium selenite/kg diet) on spermatogenesis after BPA treatment in different groups of male BALB/c mice: control, selenium, BPA and selenium+BPA. Markers of oxidative stress and apoptosis were evaluated in testis after BPA treatment. Significant decrease in sperm concentration and motility and increased reactive oxygen species(ROS) and LPO levels were seen in BPA group. Histopathological changes revealed extensive vacuolisation, lumen devoid of spermatozoa and decreased germ cell count, confirmed by testicular germ cell count studies. TUNEL assay for apoptosis showed increased number of TUNEL-positive germ cells in BPA group with increased percentage apoptotic index. However, in Se+BPA group, histopathological studies revealed systematic array of all germ cells, preserved basement membrane with relatively less vacuolisation, improved sperm parameters and ROS and LPO levels and decreased number of TUNEL-positive germ cells. These results clearly demonstrate the role of selenium in ameliorating oxidative stress and apoptosis induced upon BPA treatment in mice and can be further used as therapeutic target in male infertility.

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.