Per- and Polyfluoroalkyl Substances (PFASs) Impair Lipid Metabolism in Rana nigromaculata: A Field Investigation and Laboratory Study.

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.

[Studying the changes of the related serum complement immune indexes in patients with occupational medicamentosa-like dermatitis induced by trichloroethylene and workers occupationally exposed to trichloroethylene].

OBJECTIVE: To explore the mechanism of occupational medicamentosa-like dermatitis (OMDT) induced by trichloroethylene (TCE) and some immunity indexes in workers occupationally exposed to TCE. METHODS: The blood samples from 8 cases with medicamentosa-like dermatitis in 1st, 2nd, 3rd, 4th and 5th weeks after admitting to hospital were examined for liver function, immunoglobulin and some complement indexes. Thirty nine workers occupationally exposed to TCE were investigated for urinary TCE and some immuno-complement indexes. The TCE concentrations of air in workplaces were monitored. RESULTS: C3d-CIC and C3 of patients before admission were (92.86 ± 44.80) mg/L and 0.91 ± 0.19 mg/L, respectively. C3d-CIC and C3 of patients before discharge were (52.41 ± 17.75) mg/L and (1.14 ± 0.22) mg/L, respectively. There were significant differences between admission and discharge (P < 0.05). The average TCE concentration in 4 workplaces was (351.96 ± 36.72) mg/m(3), which was higher than the occupational exposure limits (OELs). The number of workers exposed to the TCE concentration-time weighted and TCA in urine over OELs were 28.21% and 56.41% of total subjects, respectively. The serum IgG and CIC levels of patients before discharge were (10.03 ± 1.21) mg/L and 103.50 ± 29.17 mU/L, which were significantly lower than those (17.21 ± 1.85) mg/L and (227.46 ± 111.67) mU/L of patients before admission (P < 0.01). CONCLUSION: The type II and III hypersensitivity may be associated with OMDT and the organ injure induced by TCE.