Maternal exposure to BPA during the perinatal period leads to imbalances in the testicular antioxidant enzymatic system and apoptosis in adult rat offspring.

Bisphenol A (BPA) is a widely used plasticizer that can leach from packaging, leading to contamination of food and beverages. Exposure to endocrine-disrupting chemicals during critical windows of development may lead to functional abnormalities in adulthood. Disruption of redox homeostasis and impaired activity of key antioxidant enzymes contribute to testicular dysfunction and reduced sperm quality. We evaluated the effects of perinatal BPA exposure on the testicular enzymatic antioxidant system in the adult offspring of dams treated with BPA (0.5 or 5 mg BPA/kg BW/day) from gestational day 18 throughout postnatal day (PND) 5. The testes of offspring were collected at PND90, and the transcription levels of <italic>Sod1</italic> and <italic>Gsr</italic> were reduced, those of <italic>Nfe2l2</italic> and <italic>Blc2 </italic>were increased, and those of <italic>Casp3</italic> were not altered, whereas an increased ratio of <italic>Bcl2</italic>/<italic>Bax</italic> expression was observed in the BPA5 group. An increase in SOD activity was observed in the BPA0.5 group, and a decrease in GSR activity was observed in the BPA5 group. Functional enrichment analysis revealed interactions between antioxidant genes and those involved in the hypothalamic‒pituitary‒testicular axis and spermatogenesis. These findings suggest that BPA exposure can disrupt the antioxidant defense system in male reproductive tissues, potentially leading to adverse reproductive outcomes.