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<p>Bisphenol A (BPA) is a widely used chemical compound that has been shown to exert deleterious effects on living organisms. In aquatic species, the hepatopancreas, a key organ responsible for detoxification, is susceptible to damage, which can significantly impact the health and survival of these organisms. The effects of BPA on the hepatopancreas of <i>Meretrix petechialis</i> were investigated, for which <i>M. petechialis</i> were exposed to 0-, 1-, 10-, 100-µg/L BPA for 14 d. Histopathological and ultrastructural analyses, including Hematoxylin and Eosin (H&amp;E) staining and transmission electron microscopy (TEM), revealed that BPA exposure resulted in hepatopancreatic injury, mitochondrial damage, and an abnormal increase in autophagosomes. Transcriptome analysis further identified differentially expressed genes (DEGs) significantly associated with oxidative stress, apoptosis, and ferroptosis pathways. Following BPA exposure, levels of oxidative stress markers, such as hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), malondialdehyde (MDA), and superoxide dismutase (SOD) activity increased. In addition, ferroptosis-related indicators showed notable changes with increased tissue Fe<sup>2+</sup> content and decreased glutathione peroxidase 4 (GPX4) activity. The TUNEL assay also indicated an increased abundance of apoptotic cells. Finally, qRT-PCR was performed, confirming the dysregulation of genes involved in ferroptosis, apoptosis, and autophagy. This study demonstrated that BPA exposure induces oxidative stress in <i>M. petechialis</i>, leading to histopathological damage, mitochondrial dysfunction, and an abnormal accumulation of autophagosomes, ultimately triggering the activation of ferroptosis and apoptosis pathways. These findings advanced our understanding of the toxicity mechanisms of BPA in marine bivalves and facilitated the risk assessment of BPA in aquatic environments.</p>

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Bisphenol A-induced oxidative stress mediated by mitochondrial dysfunction triggers ferroptosis and apoptosis pathways in marine clams Meretrix petechialis

  • 期刊论文

  • 发表日期：

    2026年1月14日

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  • Xiaotian Wang,
  • Zhengjia Wei,
  • Shangjie Zhou,
  • Yan Liu,
  • Pengfei Chu,
  • Xinghong Xu,
  • Long Zhu

摘要

Bisphenol A (BPA) is a widely used chemical compound that has been shown to exert deleterious effects on living organisms. In aquatic species, the hepatopancreas, a key organ responsible for detoxification, is susceptible to damage, which can significantly impact the health and survival of these organisms. The effects of BPA on the hepatopancreas of Meretrix petechialis were investigated, for which M. petechialis were exposed to 0-, 1-, 10-, 100-µg/L BPA for 14 d. Histopathological and ultrastructural analyses, including Hematoxylin and Eosin (H&E) staining and transmission electron microscopy (TEM), revealed that BPA exposure resulted in hepatopancreatic injury, mitochondrial damage, and an abnormal increase in autophagosomes. Transcriptome analysis further identified differentially expressed genes (DEGs) significantly associated with oxidative stress, apoptosis, and ferroptosis pathways. Following BPA exposure, levels of oxidative stress markers, such as hydrogen peroxide (H2O2), malondialdehyde (MDA), and superoxide dismutase (SOD) activity increased. In addition, ferroptosis-related indicators showed notable changes with increased tissue Fe2+ content and decreased glutathione peroxidase 4 (GPX4) activity. The TUNEL assay also indicated an increased abundance of apoptotic cells. Finally, qRT-PCR was performed, confirming the dysregulation of genes involved in ferroptosis, apoptosis, and autophagy. This study demonstrated that BPA exposure induces oxidative stress in M. petechialis, leading to histopathological damage, mitochondrial dysfunction, and an abnormal accumulation of autophagosomes, ultimately triggering the activation of ferroptosis and apoptosis pathways. These findings advanced our understanding of the toxicity mechanisms of BPA in marine bivalves and facilitated the risk assessment of BPA in aquatic environments.