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纳米塑料和双酚 A 单独或联合暴露会导致三疣梭子蟹的肝胰腺损伤和糖代谢紊乱。

Nanoplastics and bisphenol A exposure alone or in combination induce hepatopancreatic damage and disturbances in carbohydrate metabolism in the Portunus trituberculatus.

机构信息

School of Marine Science and Fisheries, Jiangsu Ocean University, Lianyungang, Jiangsu, 222005, China.

College of Animal Science and Technology, Yangzhou University, Yangzhou, 225000, China.

出版信息

Aquat Toxicol. 2024 Dec;277:107145. doi: 10.1016/j.aquatox.2024.107145. Epub 2024 Nov 8.

Abstract

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, 10 particles/L NPs, and a combination of 100 μg/L BPA + 10 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.

摘要

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)代表一种新型的环境污染物,这些污染物对海洋节肢动物的肝胰腺的联合毒性尚未得到充分研究。为了研究 BPA 和 NPs 共同暴露对虾夷马粪海胆肝胰腺的潜在风险,分别用 100μg/L BPA、10 个/L NPs 和 100μg/L BPA+10 个/L NPs 处理虾夷马粪海胆 21 天。组织学观察表明,共同暴露严重破坏了肝胰腺组织和线粒体结构。转录组分析显示,在不同暴露条件下有 1498 个转录本差异表达,这些转录本参与细胞过程和碳水化合物代谢等生物学过程。BPA 和 NPs 共同暴露通过增加丙酮酸激酶(PK)的活性来调节丙酮酸(PA)水平,导致组织内糖原和葡萄糖(GLU)含量的变化,从而影响糖酵解。BPA 和 NPs 共同暴露诱导的 CHI3L1、ACSS2 和 ACYP2 基因的失调可能共同调节碳水化合物代谢过程。值得注意的是,VPS4 基因的下调和 GBA1、Pin1 和 CCND2 基因的上调可能会影响细胞周期,可能会影响 BPA 和 NPs 共同暴露后的细胞增殖。这些数据表明,BPA 和 NPs 的共同暴露更具细胞毒性,并导致虾夷马粪海胆肝胰腺中碳水化合物代谢、细胞增殖和组织学损伤的变化。这些知识强调需要采取积极措施减轻这些环境污染物对人类和生态健康的不利影响,同时为相关分子机制提供有价值的见解。

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