Tetrabromobisphenol A exposure compromises antioxidant defense and mitochondrial ultrastructural damage, exacerbating hepatocellular apoptosis in Cyprinus carpio

Tetrabromobisphenol A (TBBPA), widely employed as a flame retardant in electronic products and plastics, has been routinely detected in multiple environmental matrices including aquatic compartments and sediments. The common carp ( Cyprinus carpio ), an established model organism in toxicological research, was utilized in this investigation. This study aimed to evaluate the hepatotoxic effects of varying TBBPA concentrations through histological and molecular biochemical parameter analysis. Fish were administered TBBPA at concentrations of 0, 0.005, 0.05, and 0.5 mg/L for 14 days. Collectively, this investigation demonstrated that TBBPA exposure elicits multiple pathological alterations in piscine hepatic tissue, encompassing ultrastructural damage, oxidative stress, calcium homeostasis dysregulation, and apoptosis. Histopathological analysis revealed that exposure to 0.005 mg/L TBBPA induced mitochondrial and endoplasmic reticulum swelling. Biochemical analyses demonstrated TBBPA-mediated disruption of hepatic redox homeostasis, consequently triggering lipid peroxidation. Furthermore, TBBPA exposure resulted in hepatic calcium overload, characterized by diminished Ca 2+ -ATPase activity and elevated intracellular Ca 2+ concentrations. Concurrently, TUNEL assay and qRT-PCR results indicated concentration-dependent induction of apoptosis by TBBPA. This study demonstrates hepatotoxic effects induced by environmentally relevant TBBPA concentrations while elucidating potential toxicological mechanisms in the piscine liver. These findings advance the understanding of TBBPA-mediated pathological impacts on the fish liver.