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有机氯农药会损害肝细胞中线粒体的功能，并加重脂肪酸代谢紊乱。

Organochloride pesticides impaired mitochondrial function in hepatocytes and aggravated disorders of fatty acid metabolism.

机构信息

Center of Gallbladder Disease, Shanghai East Hospital, Institute of Gallstone Disease, Tongji University School of Medicine, Shanghai, 201200, China.

State Key Laboratory of Reproductive Medicine, Institute of Toxicology, Nanjing Medical University, Nanjing, China.

出版信息

Sci Rep. 2017 Apr 11;7:46339. doi: 10.1038/srep46339.

DOI:10.1038/srep46339
PMID:28397872
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5387717/
Abstract

p,p'-dichlorodiphenyldichloroethylene (p, p'-DDE) and β-hexachlorocyclohexane (β-HCH) were two predominant organochlorine pesticides (OCPs) metabolites in human body associated with disorders of fatty acid metabolism. However, the underlying mechanisms have not been fully clarified. In this study, adult male C57BL/6 mice were exposed to low dose of p, p'-DDE and β-HCH for 8 wk. OCPs accumulation in organs, hepatic fatty acid composition, tricarboxylic acid cycle (TCA) metabolites and other metabolite profiles were analyzed. Expression levels of genes involved in hepatic lipogenesis and β-oxidation were measured. Mitochondrial function was evaluated in HepG2 cells exposed to OCPs. High accumulation of p, p'-DDE and β-HCH was found in liver and damaged mitochondria was observed under electron microscopy. Expression of genes in fatty acid synthesis increased and that in mitochondrial fatty acid β-oxidation decreased in OCPs treatment groups. OCPs changed metabolite profiles in liver tissues, varied hepatic fatty acid compositions and levels of several TCA cycle metabolites. Furthermore, MitoTracker Green fluorescence, ATP levels, mitochondrial membrane potential and OCR decreased in HepG2 cells exposed to OCPs. In conclusion, chronic exposure to OCPs at doses equivalent to internal exposures in humans impaired mitochondrial function, decreased fatty acid β-oxidation and aggravated disorders of fatty acid metabolism.

摘要

p,p'-二氯二苯二氯乙烯（p,p'-DDE）和β-六氯环己烷（β-HCH）是两种主要的有机氯农药（OCPs）代谢物，与脂肪酸代谢紊乱有关。然而，其潜在机制尚未完全阐明。在这项研究中，成年雄性 C57BL/6 小鼠暴露于低剂量的 p,p'-DDE 和 β-HCH 8 周。分析了器官中 OCPs 的积累、肝脂肪酸组成、三羧酸循环（TCA）代谢物和其他代谢物谱。测量了与肝脂肪生成和β-氧化相关的基因的表达水平。评估了 HepG2 细胞中 OCPs 暴露对线粒体功能的影响。结果发现，p,p'-DDE 和 β-HCH 在肝脏中高度积累，电镜下观察到线粒体受损。脂肪酸合成相关基因的表达增加，而 OCPs 处理组中线粒体脂肪酸β-氧化相关基因的表达减少。OCPs 改变了肝组织中的代谢物谱，改变了肝脂肪酸组成和几种 TCA 循环代谢物的水平。此外，MitoTracker Green 荧光、ATP 水平、线粒体膜电位和 OCR 在 HepG2 细胞中暴露于 OCPs 后降低。总之，慢性暴露于相当于人体内部暴露剂量的 OCPs 会损害线粒体功能，减少脂肪酸β-氧化，并加重脂肪酸代谢紊乱。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7e1/5387717/c7bc1de7ac51/srep46339-f8.jpg
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