Epigenotoxicity of Bisphenol A altered global and ten-eleven translocation-dependent DNA methylation in a non-model fish.

Bisphenol A (BPA), a widespread xenoestrogen used in polycarbonate plastics and other consumer products, is frequently detected in aquatic environments, resulting in continuous exposure of fish and other aquatic organisms. Although the toxicological effects of BPA have been extensively investigated, its epigenetic impacts in non-model teleosts remain poorly characterized. This study evaluated the effects of chronic, sublethal BPA exposure on epigenetic regulation in advanced fingerlings of Labeo rohita. Fish were exposed to BPA at 3.0, 4.5, and 6.0 mg/L for 45 days. Global DNA methylation levels were quantified, and the relative expression of key methylation- and demethylation-related genes: DNA methyltransferases (dnmts), glycine N-methyltransferase (gnmt), and ten-eleven translocation enzymes (tets) was analyzed. To further assess methylation potential, the S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH) ratio was determined as a methylation index. The BPA exposure significantly increased global DNA methylation in fish tissues and produced a dose-dependent elevation in the SAM/SAH ratio. Transcriptional analysis revealed differential regulation of dnmts, gnmt, and tets, indicating coordinated disruption of both methylation and demethylation pathways. These findings demonstrate that BPA induces epigenetic instability in L. rohita by altering DNA methylation dynamics at multiple regulatory levels. This study provides the first comprehensive, multi-tier assessment of BPA-induced epigenetic modulation in this ecologically and economically important non-model teleost, highlighting its value as a relevant model for evaluating endocrine disruptor-mediated epigenotoxicity in natural aquatic systems.