Bisphenol A (BPA) is a widely found endocrine-disrupting chemical (EDC). Nanoplastics (NPs) represent a novel environmental pollutant, and the combined toxicity of these pollutants on the hepatopancreas of marine arthropods is understudied. To investigate the potential risks associated with co-exposure to BPA and NPs on the hepatopancreas, Portunus trituberculatus was treated with 100 μg/L BPA, 104 particles/L NPs, and a combination of 100 μg/L BPA + 104 particles/L NPs for 21 days, respectively. Histological observation demonstrated that co-exposure severely damaged both hepatopancreas tissue and mitochondrial structure. Transcriptome analysis revealed that 1498 transcripts were differentially expressed under different exposure conditions, and these transcripts are involved in biological processes such as cellular processes and carbohydrate metabolism. BPA and NPs co-exposure modulate pyruvic acid (PA) levels by increasing the activity of pyruvate kinase (PK), leading to changes in glycogen and glucose (GLU) content within tissues, thus affecting glycolysis. The dysregulation of the CHI3L1, ACSS2 and ACYP2 genes induced by BPA and NPs co-exposure may collectively regulate the process of carbohydrate metabolism. Notably, the downregulation of the VPS4 gene and the upregulation of the GBA1, Pin1 and CCND2 gene may affect the cell cycle, potentially impacting cell proliferation after BPA and NPs co-exposure. These data indicate that co-exposure to BPA and NPs is more significantly cytotoxic and leads to changes in carbohydrate metabolism, cell proliferation, and histological damage in the hepatopancreas of P. trituberculatus. This knowledge emphasizes the need for proactive measures to mitigate the adverse effects of these environmental pollutants on human and ecological health while also providing valuable insights into the relevant molecular mechanisms.

中文翻译：

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纳米塑料和双酚 A 单独或联合暴露会诱导三结核 Portunus 的肝胰腺损伤和碳水化合物代谢紊乱


双酚 A （BPA） 是一种广泛存在的内分泌干扰化学物质 （EDC）。纳米塑料 （NPs） 是一种新型环境污染物，这些污染物对海洋节肢动物肝胰腺的综合毒性研究不足。为探讨肝胰腺上 BPA 和 NPs 共同暴露的潜在风险，用 100 μg/L BPA、104 颗粒/L NPs 和 100 μg/L BPA + 104 颗粒/L NPs 的组合处理三结核波图鱼 Portunus trituberculatus 分别处理 21 d。组织学观察表明，共暴露严重损害了肝胰腺组织和线粒体结构。转录组分析显示，1498 个转录本在不同暴露条件下差异表达，这些转录本参与细胞过程和碳水化合物代谢等生物过程。BPA 和 NPs 通过增加丙酮酸激酶 （PK） 的活性来共同暴露调节丙酮酸 （PA） 水平，导致组织内糖原和葡萄糖 （GLU） 含量发生变化，从而影响糖酵解。BPA 和 NPs 共暴露诱导的 CHI3L1、ACSS2 和 ACYP2 基因失调可能共同调节碳水化合物代谢过程。值得注意的是，VPS4 基因的下调以及 GBA1、Pin1 和 CCND2 基因的上调可能会影响细胞周期，从而可能影响 BPA 和 NPs 共暴露后的细胞增殖。这些数据表明，共同暴露于 BPA 和 NPs 具有更显着的细胞毒性，并导致 P. trituberculatus 肝胰腺中碳水化合物代谢、细胞增殖和组织学损伤的变化。 这些知识强调了采取积极措施来减轻这些环境污染物对人类和生态健康的不利影响的必要性，同时也为相关分子机制提供了有价值的见解。