Oxidative Damage of Bisphenol A to Meretrix petechialis Gill Tissues.

Bisphenol A (BPA) is one of the highly produced chemicals globally and extensively utilized in the manufacturing of plastic products. However, the widespread application of BPA has led to its frequent detection in aquatic environments, posing potential threats to the health of aquatic organisms. Previous studies have confirmed the reproductive and developmental toxic effects of BPA on various aquatic organisms; however, limited research exists regarding its impact on bivalve shellfish. In this study, clams ( Meretrix petechialis) were exposed to concentrations of 1, 10, and 100 μg·L^-1 BPA for 14 d. The filtration rate of gill water and histopathological changes were examined while expression levels of genes in the Nrf2/Keap1 signaling pathway and the enzymatic activity, including the hydrogen peroxide (H₂O₂) and malondialdehyde (MDA), activities of catalase (CAT), glutathione-S-transferase (GST) and superoxide dismutase (SOD) were analyzed. The results showed that BPA exposure significantly influenced the filtration rate of the clam. BPA induced epithelial cell damage and hyperplasia in the gill tissues of the clam, accompanied by a reduction in cilia and gill filaments. Notably, the gill damage became more pronounced with increasing concentrations of BPA. BPA exposure significantly increased the levels of H₂O₂ and MDA, and the oxidative stress level was the most obvious under 1 μg·L^-1 BPA exposure group. BPA exposure significantly decreased CAT activity in gill tissue, but had no significant effect on SOD activity. 1 μg·L^-1 BPA exposure resulted in a significant increase in GST activity. In addition, the gene expression levels of Nrf2, Keap1, cat, and tnf-α in the gill tissue of clams were inhibited by 1 μg·L^-1 BPA exposure. However, it is worth noting that catgene expression was upregulated specifically under 10 μg·L^-1 BPA exposure. This study reveals that BPA exposure induces oxidative stress and tissue damage in clam gill tissues. [ABSTRACT FROM AUTHOR]