Deleterious effects of decabromodiphenyl ethane on intestinal health and metabolism in zebrafish model: During the transition from maternal nutrition to exogenous nutrition

The novel brominated flame retardant, decabromodiphenyl ethane (DBDPE), is acknowledged as a disruptor of metabolic processes in biological systems. However, the specific mechanisms by which DBDPE induces metabolic disorders remain unclear, particularly during critical developmental phases, such as the transition from maternal to exogenous nutrition. In this study, zebrafish embryos were exposed to DBDPE at concentrations of 50–400 μg/L over a crucial 10-day period. Histopathological analysis revealed that exposure to DBDPE resulted in intestine structure alterations, leading to dysfunction and inflammation. Sequencing of 16S rRNA revealed that DBDPE altered the gut microbiota composition, specifically affecting the numbers of bacterial genera like Flavobacterium and Aeromonas, which cause intestinal disease. In addition, a metabolomic investigation indicated changes in metabolites mainly functioning in purine metabolism, ABC transporter, and oxidative phosphorylation. Notably, MetOrigin analysis uncovered an intriguing connection between gut bacteria (e.g., Aeromonas and Flavobacterium) and metabolites (e.g., inosine and hypoxanthine) associated with the purine metabolism pathway. Biomarker analysis corroborated these results. Overall, these findings indicated that in zebrafish larvae transitioning from maternal to exogenous nutrition, the toxic effects of DBDPE might be related to its detrimental impact on intestinal health, thereby disrupting energy metabolism processes, particularly purine metabolism.