The environmental presence of
polybrominated diphenyl ethers (
PBDEs) is ubiquitous due to their wide use as brominated
flame retardants in industrial products. As a common congener of
PBDEs,
decabromodiphenyl ether (BDE-209) can pose a health risk to animals as well as humans. However, to date, few studies have explored BDE-209's toxic effects on the intestinal tract, and its relevant mechanism of toxicity has not been elucidated. In this study, adult male zebrafish were exposed to
BDE-209 at 6 μg/L, 60 μg/L and 600 μg/L for 28 days, and intestinal tissue and microbial samples were collected for analysis to reveal the underlying toxic mechanisms. Transcriptome sequencing results demonstrated a dose-dependent pattern of substantial gene differential expression in the group exposed to
BDE-209, and the differentially expressed genes were mainly concentrated in pathways related to
protein synthesis and processing, redox reaction, and
steroid and lipid metabolism. In addition,
BDE-209 exposure caused damage to intestinal structure and barrier function, and promoted intestinal oxidative stress, inflammatory response, apoptosis and
steroid and
lipid metabolism disorders. Mechanistically,
BDE-209 induced intestinal
inflammation by increasing the levels of TNF-α and IL-1β and activating the NFκB signaling pathway, and might induce apoptosis through the p53-Bax/Bcl2-Caspase3 pathway.
BDE-209 also significantly inhibited the gene expression of rate-limiting
enzymes such as Sqle and 3βhsd (p < 0.05) to inhibit
cholesterol synthesis. In addition,
BDE-209 induced
lipid metabolism disorders through the mTOR/PPARγ/RXRα pathway.
16S rRNA sequencing results showed that
BDE-209 stress reduced the richness and diversity of intestinal microbiota, and reduced the abundance of probiotics (e.g., Bifidobacterium and Faecalibacterium). Overall, the results of this study help to clarify the intestinal response mechanism of
BDE-209 exposure, and provide a basis for evaluating the health risks of
BDE-209 in animals.