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首页> 外文期刊>Journal of cellular physiology. >Effect of hydrogen sulfide on glycolysis-based energy production in mouse erythrocytes
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Effect of hydrogen sulfide on glycolysis-based energy production in mouse erythrocytes

机译：硫化氢对glycolysis-based的影响能源生产在小鼠红细胞

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Hydrogen sulfide (H_2S) is a gasotransmitter that regulates both physiological and pathophysiological processes in mammalian cells. Recent studies have demonstrated that H_2S promotes aerobic energy production in the mitochondria in response to hypoxia, but its effect on anaerobic energy production has yet to be established. Glycolysis is the anaerobic process by which ATP is produced through the metabolism of glucose. Mammalian red blood cells (RBCs) extrude mitochondria and nucleus during erythropoiesis. These cells would serve as a unique model to observe the effect of H_2S on glycolysis-mediated energy production. The purpose of this study was to determine the effect of H_2S on glycolysis-mediated energy production in mitochondria-free mouse RBCs. Western blot analysis showed that the only H_2S-generating enzyme expressed in mouse RBCs is 3-mercaptopyruvate sulfur-transferase (MST). Supplement of the substrate for MST stimulated, but the inhibition of the same suppressed, the endogenous production of H_2S. Both exogenously administered H_2S salt and MST-derived endogenous H_2S stimulated glycolysis-mediated ATP production. The effect of NaHS on ATP levels was not affected by oxygenation status. On the contrary, hypoxia increased intracellular H2S levels and MST activity in mouse RBCs. The mitochondria-targeted H_2S donor, AP39, did not affect ATP levels of mouse RBCs. NaHS at low concentrations (3-100 μM) increased ATP levels and decreased cell viability after 3 days of incubation in vitro. Higher NaHS concentrations (300-1000 μM) lowered ATP levels, but prolonged cell viability. H_2S may offer a cytoprotective effect in mammalian RBCs to maintain oxygen-independent energy production.
机译：硫化氢(硫化氢)是一个gasotransmitter调节生理和在哺乳动物细胞病理生理过程。最近的研究表明,硫化氢促进有氧的能源生产线粒体在缺氧反应,但它影响厌氧能源生产尚未建立。通过产生ATP的过程代谢葡萄糖。(红血球)挤压线粒体和细胞核红细胞生成。独特的模型观察硫化氢的影响glycolysis-mediated能源生产。本研究的目的是确定效果glycolysis-mediated能源生产的检测在线粒体鼠标红血球。分析表明,唯一H_2S-generating酶表达的小鼠红细胞表面3-mercaptopyruvate sulfur-transferase (MST)。补充MST衬底的刺激,但相同的抑制,抑制内源性硫化氢的生产。管理检测盐和MST-derived内生硫化氢刺激glycolysis-mediated ATP生产。不受氧化影响的地位。相反,缺氧增加细胞内的硫化氢在小鼠红细胞表面水平和MST活动。AP39 mitochondria-targeted硫化氢供体,没有小鼠红细胞表面的影响ATP水平。(3 - 100μM)浓度增加ATP水平3天后,降低细胞生存能力体外孵化。(300 - 1000μM)降低了ATP的水平,但长时间细胞的生存能力。在哺乳动物红细胞表面保持效果oxygen-independent能源生产。

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