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 xenoâoestrogenic 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 BPAâinduced OS, and further germ cell death by modifying mitogenâactivated 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 BPAâtreated animals demonstrated a marked decrease in antioxidant enzyme activities (superoxide dismutase, catalase, redox ratio), a marked elevation in the expressions of stressâactivated kinases (câJun NH2âterminal kinase (JNK), extracellular signalâregulated kinase (ERK) and p38) and the expressions of proâapoptotic markers (caspaseâ9, caspaseâ8 and caspaseâ3). However, Se supplementation considerably restored the antioxidant enzyme activities and lowered the expressions of stressâactivated kinases, which further downâregulated the apoptosis. Thus, Se supplementation demonstrated to be effective against BPA provoked testicular damage.