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

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, 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.