Per- and polyfluoroalkyl substances (PFASs) are ubiquitous
environmental
pollutants, causing environmental threats and public health concerns,
but information regarding PFAS hepatotoxicity remains elusive. We
investigated the effects of PFASs on lipid metabolism in black-spotted
frogs through a combined field and laboratory study. In a fluorochemical
industrial area, PFASs seriously accumulate in frog tissues. PFAS
levels in frog liver tissues are positively related to the hepatosomatic
index along with triglyceride (TG) and cholesterol (TC) contents.
In the laboratory, frogs were exposed to 1 and 10 μg/L PFASs,
respectively (including PFOA, PFOS, and 6:2 Cl-PFESA). At 10 μg/L,
PFASs change the hepatic fatty acid composition and significantly
increase the hepatic TG content by 1.33 to 1.87 times. PFASs induce
cross-talk accumulation of TG, TC, and their metabolites between the
liver and serum. PFASs can bind to LXRα and PPARα proteins,
further upregulate downstream lipogenesis-related gene expression,
and downregulate lipolysis-related gene expression. Furthermore, lipid
accumulation induced by PFASs is alleviated by PPARα and LXRα
antagonists, suggesting the vital role of PPARα and LXRα
in PFAS-induced lipid metabolism disorders. This work first reveals
the disruption of PFASs on hepatic lipid homeostasis and provides
novel insights into the occurrence and environmental risk of PFASs
in amphibians.
Biochar is an effective amendment for trace metals/metalloids (TMs) immobilization in soils. The capacity of biochar to immobilize TMs in soil can be positively or negatively altered due to the...
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