Abstract
Bisphenol A (BPA) is one of the most common environmental endocrine disruptor chemicals (EDCs) and exhibits reproductive, cardiovascular, immune, and neurodevelopmental toxic effects. The development of the offspring was examined in the present investigation to determine the cross-generational effects of long-term exposure of parental zebrafish to environmental concentrations of BPA (15 and 225µg/L). Parents were exposed to BPA for 120days, and their offspring were evaluated at 7days after fertilization in BPA-free water. The offspring exhibited higher mortality, deformity, and heart rates, and showed significant fat accumulation in abdominal region. RNA-Seq data showed that more lipid metabolism-related KEGG pathways, such as the PPAR signaling pathway, adipocytokine signaling pathway, and ether lipid metabolism pathway were enriched in the 225µg/LBPA-treated offspringcompared to15µg/LBPA-treated offspring, indicating greater effects of high doseBPA on offspring lipid metabolism. Lipid metabolism-related genes implied that BPA is responsible for disrupting lipid metabolic processes in the offspring through increased lipid production, abnormal transport, and disruption of lipid catabolism. The present study will be helpful for further evaluation of the reproductive toxicity of environmental BPA to organisms and thesubsequentparent-mediated intergenerational toxicity.
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