Decabromodiphenyl ethane (DBDPE), a chemical compound widely detected in aquatic ecosystems, has shown a range of toxicological effects in zebrafish ( Danio rerio ). However, its effects on zebrafish reproduction remain underexplored. In this study. Adult zebrafish were exposed to 0, 1, 10, and 100 μg/L of DBDPE for 21 days. DBDPE accumulated in the gonads, leading to a marked decrease in both cumulative spawning and gonadosomatic index in female zebrafish. To investigate the mechanisms underlying reproductive abnormalities induced by DBDPE, we measured serum hormone levels, oocyte development, and gene expression in the hypothalamic–pituitary–gonadal (HPG) axis. Our results showed that exposure to DBDPE significantly reduced estradiol (E2) levels in female zebrafish, along with abnormal oocyte development and disrupted gene expression in the HPG axis. Further metabolomic and lipidomic analyses revealed considerable changes in taurine and hypotaurine metabolism, glutathione metabolism, and the FoxO signaling pathway, along with significant disturbances in lipid metabolism. These disruptions in metabolic pathways may be an important underlying cause of delayed oocyte development. Our findings show that exposure to DBDPE delays oocyte development by altering lipid metabolism, reducing sex hormone levels, and impairing HPG axis regulation, ultimately leading to reduced fecundity in female zebrafish. This study highlights the repercussions of DBDPE exposure on the reproductive health of zebrafish, emphasizing the need for stricter regulation of its production and use, a well as a comprehensive reassessment of the risks it poses to fish.
Yu et al. (Sun,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: