This study examines the sex-specific effects of gestational exposure (days 6–21) to endocrine-disrupting chemicals such as bisphenol A (BPA), diethylhexyl phthalate (DEHP), or their combination on brain monoamine levels that play an important role in regulating behavior. Pregnant Sprague–Dawley rats were orally administered saline, low doses (5 µg/kg BW/day) of BPA or DEHP, and their combination or a high dose (7.5 mg/kg BW/day) of DEHP alone or in combination with BPA during pregnancy. The offspring were subjected to a behavioral test and sacrificed in adulthood, and the brains were analyzed for neurotransmitter levels. In the paraventricular nucleus, there was a marked reduction in dopamine levels (p < 0.01) in male offspring from the BPA, DEHP, and B + D (HD) groups, which correlated well with their shock probe defensive burying times. Neurotransmitter changes in all brain regions examined were significant in female offspring, with DEHP (HD) females being affected the most, followed by the B + D groups. BPA and/or DEHP (LD) increased monoamine turnover in a region-specific manner in male offspring (p < 0.05). Overall, prenatal exposure to BPA, DEHP, or their combination alters monoamine levels in a brain region-specific, sex-specific, and dose-dependent manner, which could have implications for their behavioral and neuroendocrine effects.

This study investigates the metabolic parameters of prenatal exposure to low doses of Bisphenol A (BPA) and its analogues, BPS and BPF, and the subsequent effects of high-fat diet (HFD) challenge in offspring during adulthood. Pregnant Sprague Dawley rats received saline (control), BPA or BPS (5 µg/kg BW), or BPF (1 µg/kg BW) via oral gavage from gestation days 6–21. Offspring growth, fat deposition, glucose tolerance, insulin, corticosterone, and cholesterol levels were measured in male and female offspring. Prenatal BPA exposure reduced food intake in males and induced pronounced glucose excursions in chow-fed females, which improved over time. In males, BPA caused a rapid 30-min glucose spike and increased body weight, fat, and lean mass following HFD. BPS exposure resulted in mild postnatal growth retardation and reduced food intake in chow-fed females, while males showed increased fluid mass. BPS females exhibited sharp glucose declines after 2 weeks, and HFD led to reduced brown adipose tissue. In males, BPS increased liver and serum cholesterol following HFD. BPF exposure increased water intake and led to greater fat accumulation after HFD, along with reduced fluid mass in males. HFD increased adiposity across groups, with sex-specific differences in body composition but no major effects on glucose tolerance. These findings demonstrate that low-dose prenatal exposure to BPA analogues alters metabolic parameters in offspring, with sex- and compound-specific effects, which can be modulated by dietary challenge.