Oxidation of hydrogen sulfide remains a priority in mammalian cells and causes reverse electron transfer in colonocytes
Oxidation of hydrogen sulfide remains a priority in mammalian cells and causes reverse electron transfer in colonocytes
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DOI：
10.1016/j.bbabio.2010.04.004
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发表时间：
2010-08-01
影响因子：
4.3
通讯作者：
Bouillaud, Frederic
中科院分区：
文献类型：
--
作者：
Lagoutte, Emilie;Mimoun, Sabria;Bouillaud, Frederic
硫化物（H₂S）是一种与氰化物相当的线粒体细胞色素氧化酶抑制剂。在这项研究中，观察到硫化物浓度高于20μM时细胞会中毒。已表明在自然暴露于硫化物的生物体/细胞中会发生硫化物氧化。硫化物是含硫氨基酸代谢的结果而释放出来的。尽管在哺乳动物中，除结肠黏膜外，硫化物暴露在数量上被认为并不重要，但我们的研究表明，大多数哺乳动物细胞通过线粒体硫化物醌还原酶（SQR），积极地将硫化物作为燃料消耗。在从小鼠肾脏、肝脏和心脏分离出的线粒体中发现了SQR活性。我们证明了SQR优先于线粒体复合物I。这就解释了为什么矿物质底物硫化物的氧化优先于其他（碳基）线粒体底物的氧化。因此，如果硫化物输送速率保持低于SQR活性，细胞内就会维持一个无毒的硫化物浓度（
Sulfide (H2S) is an inhibitor of mitochondrial cytochrome oxidase comparable to cyanide. In this study, poisoning of cells was observed with sulfide concentrations above 20 mu M. Sulfide oxidation has been shown to take place in organisms/cells naturally exposed to sulfide. Sulfide is released as a result of metabolism of sulfur containing amino acids. Although in mammals sulfide exposure is not thought to be quantitatively important outside the colonic mucosa, our study shows that a majority of mammalian cells, by means of the mitochondrial sulfide quinone reductase (SQR), avidly consume sulfide as a fuel. The SQR activity was found in mitochondria isolated from mouse kidneys, liver, and heart. We demonstrate the precedence of the SQR over the mitochondrial complex I. This explains why the oxidation of the mineral substrate sulfide takes precedence over the oxidation of other (carbon-based) mitochondria! substrates. Consequently, if sulfide delivery rate remains lower than the SQR activity, cells maintain a non-toxic sulfide concentration (