The impact of bisphenol A on gill health: A focus on mitochondrial dysfunction induced disorders of energy metabolism and apoptosis in Meretrix petechialis.

Bisphenol A (BPA), a well-known chemical compound used in various daily goods, has been associated with adverse effects on animal metabolic processes. However, the specific impacts of BPA exposure on clam gills remain largely unexplored. To investigate the effects of BPA on energy metabolism and apoptosis in Meretrix petechialis gills, clams were exposed to varying concentrations of BPA (1, 10, and 100 μg/L) for 21 days. Results showed that BPA exposure induced gill histopathological injuries and inhibited filtration rates. Transmission electron microscopy (TEM) analysis revealed mitochondrial injury and dysfunction as potential mechanisms of gill damage. Transcriptome analysis identified differentially expressed genes (DEGs) primarily enriched in energy metabolism and apoptosis pathways. BPA-induced changes in ATP content, ATPase, and lactate dehydrogenase (LDH) activities suggested dysregulation of energy metabolism. TUNEL staining demonstrated enhanced apoptotic signals with increasing BPA concentrations. Activation of the caspase-3/9 pathway indicated a concentration-dependent, mitochondria-dependent apoptotic process. Additionally, the expression of genes associated with mitochondria (NNT, TOMM40, and SLC25A11), energy metabolism (PCK1 and pdhC), inducing mitochondria-dependent apoptosis (NFKB1, RAC1, and TRAF2), and oxidative stress (GSTT1) was affected by BPA exposure. Integrated biomarker response version 2 (IBRv2) values further confirmed a concentration-dependent gill toxicity of BPA via the mitochondrial pathway. These findings provide a deeper understanding of the toxicological mechanisms underlying BPA-induced toxicity in bivalves and contribute to assessing the risks posed by BPA in benthic ecosystems.