Tetrabromobisphenol a and its alternative tetrachlorobisphenol a induce oxidative stress, lipometabolism disturbance, and autophagy in the liver of male Pelophylax nigromaculatus

Han, Yu; Yang, Hongmei; Liu, Zhiqun; Hu, Chao; Lamine, Imane; Liu, Zhiquan; Gao, Panpan; Sui, Yanming; Zheng, Pei; Zhang, Hangjun; Jia, Xiuying

doi:10.1016/j.scitotenv.2023.166421

Cited by 5 publications

(1 citation statement)

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“…In the past decade, increasing evidence has shown that autophagy is involved in hepatic lipid metabolism and the pathogenesis of NAFLD. , For example, B[a]P exposure promotes lipid deposition in primary hepatocytes by inhibiting autophagy, leading to lipid accumulation and finally hepatic steatosis in mice . A previous study suggested that exposure to tetrabromobisphenol A and tetrachlorobisphenol A enhances cellular autophagy, promotes TC and TG accumulation, raise oxidative stress, and increases AST/ALT activity in the liver of black-spotted frogs (Pelophylax nigromaculatus) . Our lipidomic and transcriptomic results are supported by these observations and add evidence for the associations between TBPH-induced hepatic lipid metabolic disorders and cellular autophagy in zebrafish larvae.…”

Section: Resultsmentioning

confidence: 99%

Bis(2-ethylhexyl)-2,3,4,5-tetrabromophthalate Enhances foxo1-Mediated Lipophagy to Remodel Lipid Metabolism in Zebrafish Liver

Zhou,

Li,

et al. 2024

Environ. Sci. Technol.

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An emerging environmental contaminant, bis(2-ethylhexyl)-2,3,4,5tetrabromophthalate (TBPH), can bioaccumulate in the liver and affect hepatic lipid metabolism. However, the in-depth mechanism has yet to be comprehensively explored. In this study, we utilized transgenic zebrafish Tg (Apo14: GFP) to image the interference of TBPH on zebrafish liver development and lipid metabolism at the early development stage. Using integrated lipidomic and transcriptomic analyses to profile the lipid remodeling effect, we uncovered the potential effects of TBPH on lipophagy-related signaling pathways in zebrafish larvae. Decreased lipid contents accompanied by enhanced lipophagy were confirmed by the measurements of Oil Red O staining and transmission electron microscopy in liver tissues. Particularly, the regulatory role of the foxo1 factor was validated via its transcriptional inhibitor. Double immunofluorescence staining integrated with biochemical analysis indicated that the enhanced lipophagy and mitochondrial fatty acid oxidation induced by TBPH were reversed by the foxo1 inhibitor. To summarize, our study reveals, for the first time, the essential role of foxo1-mediated lipophagy in TBPH-induced lipid metabolic disorders and hepatoxicity, providing new insights for metabolic disease studies and ecological health risk assessment of TBPH.

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