Gilliland F D, Mandel J S
Division of Environmental and Occupational Health, School of Public Health, University of Minnesota, Minneapolis, USA.
Am J Ind Med. 1996 May;29(5):560-8. doi: 10.1002/(SICI)1097-0274(199605)29:5<560::AID-AJIM17>3.0.CO;2-Z.
Perfluorooctanoic acid (PFOA) produces marked hepatic effects, including hepatomegaly, focal hepatocyte necrosis, hypolipidemia, and alteration of hepatic lipid metabolism in a number of animal species. In rodents, PFOA is a peroxisome proliferator, an inducer of members of the cytochrome P450 superfamily and other enzymes involved in xenobiotic metabolism, an uncoupler of oxidative phosphorylation, and may not be a cancer promoter. Although PFOA is the major organofluorine compound found in humans, little information is available concerning human responses to PFOA exposure. This study of 115 occupationally exposed workers examined the cross-sectional associations between PFOA and hepatic enzymes, lipoproteins, and cholesterol. The findings indicate that there is no significant clinical hepatic toxicity at the PFOA levels observed in this study. PFOA may modulate the previously described hepatic responses to obesity and xenobiotics.
全氟辛酸（PFOA）会对肝脏产生显著影响，包括肝肿大、局灶性肝细胞坏死、低脂血症以及多种动物物种肝脏脂质代谢的改变。在啮齿动物中，PFOA是一种过氧化物酶体增殖剂，是细胞色素P450超家族成员及其他参与外源性物质代谢的酶的诱导剂，是氧化磷酸化的解偶联剂，且可能不是癌症促进剂。尽管PFOA是在人类体内发现的主要有机氟化合物，但关于人类对PFOA暴露的反应，目前所知甚少。这项针对115名职业暴露工人的研究，考察了PFOA与肝酶、脂蛋白和胆固醇之间的横断面关联。研究结果表明，在本研究观察到的PFOA水平下，不存在显著的临床肝脏毒性。PFOA可能会调节先前描述的肝脏对肥胖和外源性物质的反应。
