Schnellmann R G, Ewell F P, Sgambati M, Mandel L J
Department of Physiology and Pharmacology, College of Veterinary Medicine, University of Georgia, Athens 30602.
Toxicol Appl Pharmacol. 1987 Sep 30;90(3):420-6. doi: 10.1016/0041-008x(87)90134-7.
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 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 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 translocator and/or the F1-ATPase.
2-溴对苯二酚（BHQ）是溴苯的一种肾毒性代谢产物，也是一种典型的有毒对苯二酚。这些研究的主要目的是确定BHQ是否通过抑制线粒体功能在兔肾近端小管中产生毒性。BHQ会引发特定的细胞事件序列。最初，肾小管谷胱甘肽含量降低，随后制霉菌素刺激的哇巴因敏感呼吸作用减弱。通过乳酸脱氢酶保留率降低来衡量的细胞活力下降是较晚出现的事件。与呼吸作用减弱相关的是细胞内ATP含量降低。对肾小管线粒体功能的探究表明，BHQ确实以某种选择性方式抑制了线粒体功能。在通过细胞色素c - 细胞色素氧化酶的电子流速率发生变化之前，状态3呼吸就受到了抑制。据推测，BHQ可能最初通过抑制腺嘌呤核苷酸转位酶和/或F1 - ATP酶来抑制状态3呼吸。
