硫化氢的氧化在哺乳动物细胞中仍然是一个优先事项，并导致结肠细胞中的反向电子转移

Oxidation of hydrogen sulfide remains a priority in mammalian cells and causes reverse electron transfer in colonocytes

 

 

 

Keywords：Mitochondria,Sulfide quinone reductase,Mitochondrial complex I, Detoxification,Stoichiometry
关键词：线粒体，硫化醌还原酶，线粒体复合物 I,解毒，化学计量

细胞系：CHO细胞系（中国仓鼠卵巢细胞系）
作者：Lagoutte E, Mimoun S, Andriamihaja M, Chaumontet C, Blachier F, Bouillaud F
出版期刊：《Biochimica et Biophysica Acta》 2010/4/14

Abstract：

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 µM. 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) mitochondrial substrates. Consequently, if sulfide delivery rate remains lower than the SQR activity, cells maintain a non-toxic sulfide concentration (b1 µM) in their external environment. In the colonocyte cell line HT-29, sulfide oxidation provided the first example of reverse electron transfer in living cells, such a transfer increasing sulfide tolerance. However, SQR activity was not detected in brain mitochondria and neuroblastoma cells. Consequently, the neural tissue would be more sensitive to sulfide poisoning. Our data disclose new constraints concerning the emerging signaling role of sulfide.

 

文章摘要：

硫化物 (H2S) 是一种线粒体细胞色素氧化酶抑制剂，可与氰化物相媲美。在这项研究中，当硫化物浓度高于 20 µM 时观察到细胞中毒。硫化物氧化已被证明发生在自然暴露于硫化物的生物体/细胞中。硫化物由于含硫氨基酸的代谢而释放。尽管在哺乳动物中，硫化物暴露在结肠粘膜以外的数量上并不重要，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 ), 大量消耗硫化物作为燃料。在从小鼠肾脏、肝脏和心脏分离的线粒体中发现了 SQR 活性。我们证明了 SQR 优先于线粒体复合物 I。这解释了为什么矿物底物硫化物的氧化需要优先于其他（碳基）线粒体底物的氧化。因此，如果硫化物输送速率仍然低于SQR活性，细胞在其外部环境中保持无毒的硫化物浓度 (b1 µM)。在结肠细胞系 HT-29 中，硫化物氧化提供了活细胞中反向电子转移的第一个例子，这种转移增加了硫化物耐受性。然而，在脑线粒体和神经母细胞瘤细胞中未检测到 SQR 活性。因此，神经组织对硫化物中毒更敏感。我们的数据揭示了关于硫化物新兴信号作用的新限制。

 

 

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