Accumulation of perfluorobutanesulfonate (PFBS) is frequently detected in biota, raising concerns about its ecological safety. However, hazardous effects of PFBS remain largely unexplored, especially for endocrine disrupting potency. In the present study, the multigenerational endocrine disrupting potential of PFBS was investigated by exposing F0 marine medaka eggs to PFBS at different concentrations (0, 1.0, 2.9, and 9.5 μg/L) until sexual maturity. The F1 and F2 generations were reared without continued exposure. Thyroidal disturbances were examined in all three generations. PFBS exposure decreased the levels of 3,5,3'-triiodothyronine (T3) in F0 female blood; however, it increased T3 or thyroxine (T4) levels in F0 brains, in which hyperthyroidism suppressed the local transcription of 5'-deiodinase 2 ( Dio2). Obviously decreased T3 was transferred to F1 eggs, although the parental influences were reversed in F1 larvae. Delayed hatching was coupled with elevated T3 levels in F1 larvae. F1 adults showed comparable symptoms of thyroidal disruption with F0 adults. A slight recovery was noted in the F2 generation, although F2 larvae still exhibited thyroid disruption and synthesized excessive T4. Our results suggested that the offspring suffered more severe dysfunction of the thyroidal axis albeit without direct exposure. This study provided the first molecular insight about PFBS toxicology on the thyroid, beneficial to both human and environmental risk assessment.
Hypoxia is a pressing environmental
problem in both marine and
freshwater ecosystems globally, and this problem will be further exacerbated
by global warming in the coming decades. Recently, we reported that
hypoxia can cause transgenerational impairment of sperm quality and
quantity in fish (in F0, F1, and F2 generations) through DNA methylome
modifications. Here, we provide evidence that female fish (Oryzias melastigma) exposed to hypoxia exhibit reproductive
impairments (follicle atresia and retarded oocyte development), leading
to a drastic reduction in hatching success in the F2 generation of
the transgenerational group, although they have never been exposed
to hypoxia. Further analyses show that the observed transgenerational
impairments in ovarian functions are related to changes in the DNA
methylation and expression pattern of two gene clusters that are closely
associated with stress-induced cell cycle arrest and cell apoptosis.
The observed epigenetic and transgenerational alterations suggest
that hypoxia may pose a significant threat to the sustainability of
natural fish populations.
To determine how the aryl hydrocarbon receptor (AhR) signaling acts along the gut−liver axis, we employed an integrated metagenomic and metabolomic approach to comprehensively profile the microbial and metabolic networks. Adult zebrafish were exposed to a model agonist of the AhR: polychlorinated biphenyl (PCB) 126. The metagenomic analysis showed that PCB126 suppressed microbial activities related to primary bile acid metabolism in male intestines. Accordingly, a suite of primary bile acids consistently showed higher concentrations, suggesting that bacterial conversion of primary bile acids was blocked. PCB126 also disturbed bacterial metabolism of bile acids in female intestines, as revealed by higher concentrations of primary bile acids (e.g., chenodeoxycholic acid) and activation of the nuclear farnesoid X receptor signaling. In addition, PCB126 exposure impaired the metabolism of various essential vitamins (e.g., retinol, vitamin B6, and folate). Degradation of vitamin B6 by bacterial enzymes was inhibited in male intestines, resulting in its intestinal accumulation. However, PCB126 suppressed the bacterial metabolism of vitamins in female intestines, causing systematic deficiency of essential vitamins. Overall, we found that PCB126 exposure dysregulated gut microbial activities, consequently interrupting bile acid and vitamin metabolism along the gut−liver axis. The findings provided an insight of the AhR action in microbe-host metabolic communication related to PCBs.
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