Dysfunction of liver-gut axis in marine medaka exposed to hypoxia and perfluorobutanesulfonate

With objectives to explore the interactive mode on the function of liver-gut axis, adult marine medaka were exposed for 7 days to environmentally realistic concentrations of perfluorobutanesulfonate (PFBS) (0 and 10 μg/L) under normoxia or hypoxia condition. Furthermore, PFBS exposure was extended to 21 days to reveal the temporal progression in toxicity. The results showed that hypoxia exposure significantly disturbed lipid metabolism, caused oxidative damage, and induced inflammation in the livers of medaka. The composition of gut microbiota was also drastically shifted by hypoxia acute exposure. In contrast, the effect of PFBS was much milder. Hypoxia was thus the determinant of the combined toxicity. Depending on the exposure duration, a time-course recovery from PFBS innate toxicity was generally noted. Overall, the present study underlines the hypoxic and temporal variation in the dysregulation of liver-gut axis by PFBS, which is expected to support a comprehensive ecological risk assessment. [Display omitted] •Accumulation of various lipid metabolites was caused by hypoxia in blood and liver.•A temporal transition in PFBS innate toxicity was noted.•Hypoxia induced severe oxidative damage and inflammation in medaka liver.•Hypoxia and PFBS potently disrupted the composition of gut microbiota.•Hypoxia largely shaped the ultimate toxic outcome of coexposure scenario.