BDE-47 induces oxidative stress and apoptosis by interfering with pyruvate and glutathione metabolism in Epinephelus coioides

Abstract

2,2',4,4'-Tetrabromodiphenyl ether (BDE-47) is one of the most toxic and widely distributed environmental pollutants, posing a potential threat to Epinephelus coioides aquaculture in China. However, there is currently no information on the toxic effects and mechanisms of BDE-47 on E. coioides. In this study, a 14-day gavage experiment was conducted using BDE-47 on E. coioides, and related indicators were detected by H&E staining, enzyme activity detection, and qPCR. The H&E staining results showed that BDE-47 caused inflammatory infiltration and cell damage in the liver tissue of E. coioides. The enzyme activity detection and qPCR results indicated a decrease in the antioxidant capacity of liver tissue, oxidative damage, and apoptosis. In addition, the in vitro experiments showed that BDE-47 induced an increase in ROS levels and apoptosis. To further explore the toxic mechanism of BDE-47, we conducted transcriptome sequencing analysis. The GO enrichment results suggest that BDE-47 may have an impact on mitochondrial function. The KEGG enrichment results showed that most of the DEGs were enriched in KEGG signaling pathways closely related to mitochondrial function and cellular antioxidant capacity, including pyruvate metabolism, TCA cycle, and glutathione metabolism. These results suggest that BDE-47 inhibit cellular antioxidant capacity by interfering with normal mitochondrial function, resulting in oxidative damage and apoptosis. This study provides a theoretical basis and data support for the control and management of BDE-47 in fishery water environments.