Bisphenol A and Its Analogs: Toxicity Analysis in Mouse and Rat Liver—A Review

Bisphenol A (BPA) and its analogs are widely recognized for their use in industry and plastic manufacturing. Consequently, humans and animals are continually exposed to various substances in their daily lives. This review evaluates the hepatic toxicity of BPA and its analogs in mice and rats, with particular emphasis on molecular mechanisms, histopathological alterations, and interspecies differences. Studies indicate that BPA induces increased hepatotoxicity by disrupting key cellular processes, including oxidative stress, inflammation, apoptosis, and lipid metabolism. The reduction in antioxidant enzyme activities, dysregulated activation of the NRF2 pathway, imbalance in the BAX/BCL-2 ratio, and upregulation of lipogenic genes led to structural and functional abnormalities in the liver. Histopathologically, vacuolization, sinusoidal dilation, inflammatory cell infiltration, and fibrosis are among the most frequently reported findings. Although BPA analogs are often promoted as safer alternatives, current evidence indicates that this assumption is not accurate. Taken together, the conclusions of these studies demonstrate that bisphenol exposure poses a significant risk to liver health, underscoring the need to reassess the use of these compounds.