Mitochondrial toxicity of 2-bromohydroquinone in rabbit renal proximal tubules.
Mitochondrial toxicity of 2-bromohydroquinone in rabbit renal proximal tubules.
复制标题
2-溴氢醌对兔肾近曲小管的线粒体毒性。
DOI：
10.1016/0041-008x(87)90134-7
复制
发表时间：
1987
影响因子：
3.8
通讯作者：
Mandel,LJ
中科院分区：
文献类型：
--
作者：
Schnellmann,RG;Ewell,FP;Sgambati,M;Mandel,LJ
2-溴对苯二酚(BHQ)是溴苯的肾毒性代谢物，是一种典型的毒性对苯二酚。这些研究的主要目的是确定BHQ是否通过抑制线粒体功能对兔肾近端小管产生毒性。BHQ诱导一系列特定的细胞事件。最初，随着制霉菌素刺激哇巴因敏感呼吸的减少，肾小管谷胱甘肽含量降低。以乳酸脱氢酶保留率的下降来衡量细胞活力的下降是一个晚期事件。与呼吸减少相关的是细胞内ATP含量的减少。对肾小管线粒体功能的检测显示，BHQ确实在一定程度上选择性地抑制了线粒体功能。在通过细胞色素c-细胞色素氧化酶的电子流量改变之前，状态3的呼吸被抑制。推测BHQ最初可能通过抑制腺嘌呤核苷酸易位来抑制状态3呼吸。和/或F1-ATPase。
2-Bromohydroquinone (BHQ) is a nephrotoxic metabolite of bromobenzene and a model toxic hydroquinone. The primary goal of these studies was to determine whether BHQ produces toxicity in rabbit renal proximal tubules by inhibiting mitochondrial function. BHQ induces a specific sequence of cellular events. Initially there was a decrease in tubular glutathione content followed by a decrease in nystatin-stimulated ouabain-sensitive respiration. A decrease in cell viability, as measured by a decrease in lactate dehydrogenase retention, was a late event. Associated with the decrease in respiration was a decrease in intracellular ATP content. Probing of mitochondrial function in the tubule revealed that BHQ did inhibit mitochondrial function in a somewhat selective manner. State 3 respiration was inhibited prior to changes in the rate of electron flow through cytochrome c-cytochrome oxidase. It is postulated that BHQ may initially inhibit state 3 respiration by inhibiting the adenine nucleotide transloca. and/or the F1-ATPase.