期刊
TOXICOLOGY LETTERS
卷 129, 期 1-2, 页码 23-32出版社
ELSEVIER SCI IRELAND LTD
DOI: 10.1016/S0378-4274(01)00466-0
关键词
peroxisome proliferators; perfluorooctanoic acid (PFOA); perfluorooctanesulfonate (PFOS); N-ethyl perfluorooctanesulfonamido ethanol (N-EtFOSE); mitochondrial DNA (mtDNA) copy number mitochondrial biogenesis
类别
Compounds that cause peroxisome proliferation in rats and mice have been reported to interfere with mitochondrial (mt) bioenergetics and possibly biogenesis, The purpose of this investigation was to establish whether proliferation of peroxisomes and mitochondria are necessarily related. Perfluorooctanesulfonate (PFOS) and N-ethyl perfluorooetanesulfonamido ethanol (N-EtFOSE) were investigated as peroxisome proliferators in comparison to perfluorooctanoic acid (PFOA). Three parameters were chosen to assess peroxisome proliferation. stimulation of lauroyl CoA oxidase activity, reduction of serum cholesterol concentration, and hepatomegaly. mt Biogenesis was assessed through cytochrome oxidase activity, cytochrome content and mitochondrial DNA (mtDNA) copy number. PFOA, PFOS, or N-EtFOSE was administered via a single i.p. injection at 100 mg/kg in male rats., and measurements were made 3 days later. In this model. PFOS and PFOA share similar potencies as peroxisome proliferators. whereas N-EtFOSE showed no activity. mt Endpoints were altered only in the PFOA treatment group, which consisted of a decrease cytochrome oxidase activity in liver tissue and an increase in the mtDNA copy number. None of the perfluorooctanoates significantly altered mt cytochrome content following acute in vivo treatment. These data demonstrate that acute administration of PFOS or PFOA causes hepatic peroxisome proliferation in rats. However. stimulation of mt biogenesis is not a characteristic response of all peroxisome proliferators. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据