Bisphenol S (polyethersulfone, BPS) is a substitute for the industrial chemical Bisphenol A in some commercial products, including paper receipts and protective coatings inside food cans available to all age groups. Hence, there are public health concerns regarding the exposure of the population to BPS. The current literature evidently indicates that a profound surge in pro-oxidants, pro-apoptotic, and pro-inflammatory biomarkers in combination with diminished mitochondrial function can potentially decrease the hepatic function leading to morbidity and mortality. Currently, the postnatal impact of BPS on hepatocellular function and the molecular mechanisms associated with the effects of BPS in the liver is unknown. Therefore, the current study investigated the postnatal effect of BPS on the biomarkers of hepatocellular functions in rats. BPS (5 micrograms/L of drinking water) was fed to 21-day-old male Long-Evans rats for 14 days. Since BPS was dissolved in DMSO (0.001%), the control animals were provided with DMSO in drinking water at 0.001% for 14 days. All animals were sacrificed at 35 days of age. The biomarkers of oxidative stress (Reactive Oxygen Species, Nitrite, Glutathione, and Lipid Peroxide Content), inflammation (Interleukin Converting Enzyme-1 (ICE-1) activity), apoptosis (caspase-3 activity), and mitochondrial function (NADH content) were measured in the liver from control and BPS treated rats. Statistical analysis was performed using Prism-V software. Additionally, in silico analyses were conducted with SwissADME software to study the physicochemical properties of BPS. BPS had no significant effect on the markers of apoptosis, inflammation, and mitochondrial function. However, BPS significantly reduced the reactive oxygen species without affecting the nitrite and glutathione content. The in-silico analysis indicated that BPS is effectively absorbed in the gastrointestinal tract. More importantly, BPS is not an inhibitor of p-Glycoprotein and Cytochrome P-450 enzymes. Together, the present results demonstrated that short term developmental exposures to BPS had no significant hepatotoxicity in growing male rats although additional studies are warranted to determine effects due to chronic BPS exposures and/or in the adult