脂质代谢
溶血磷脂酰胆碱
磷脂酰乙醇胺
脂肪酸代谢
化学
β氧化
脂肪酸
氧化应激
新陈代谢
脂肪变性
脂质信号
肉碱
脂代谢紊乱
磷脂酰胆碱
生物化学
脂肪肝
生物
内分泌学
内科学
受体
磷脂
血脂
胆固醇
医学
疾病
膜
作者
Huang Wei,Peisi Xie,Zongwei Cai
标识
DOI:10.1016/j.jhazmat.2019.121310
摘要
Previous in vivo exposure studies focused mainly on nuclear receptors involved in hepatotoxicity of triclosan (TCS). As liver plays a vital role in metabolic processes, dysregulations in lipid metabolism have been identified as potential drivers of pathogenesis. Investigation of changes in lipid metabolism might widen our understanding of toxicological effects as well as the underlying mechanism occurring in the liver. In this study, we comprehensively assessed the effect of TCS exposure on hepatic lipid metabolism in mice. Our results showed that TCS induced significant changes in hepatic free fatty acid pool by upregulation of fatty acid uptake and de novo fatty acid synthesis. Besides, hepatic levels of lipids, including acyl carnitine (AcCa), ceramide (Cer), triacylglycerols (TG), phosphatidylcholine (PC), lysophosphatidylcholine (LPC), phosphatidylethanolamine (PE) were also increased, together with upreguation of genes associated to TG synthesis, fatty acid oxidation and inflammation in TCS exposure group. These changes in lipid homeostasis could contribute to membrane instability, lipid accumulation, oxidative stress and inflammation. Our results suggested that TCS exposure could induce hepatic lipid metabolism disorders in mice, which would further contribute to the liver damage effects of TCS.
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