硫循环的生命演化:从古代单质硫还原和硫化物氧化到当代硫醇氧化还原的挑战

R. Burini, H. Kano, Yong‐ming Yu
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引用次数: 4

摘要

生物进化导致了代谢途径的创新,其中许多无疑改变了地球表面的化学成分。火山活动引入了无机碳(h2、co2、ch4、so2和h2s),推动了古细菌和细菌领域的早期生物的代谢。在没有光的情况下,硫化氢和铁是主要的电子供体,电子受体可以是硫、硫酸盐和单质硫等氧化物质,也可以是醋酸酯发酵产生的二氧化碳(形成甲烷)。单质硫是由h2s和so2反应产生的,而无氧光合作用可能提供了硫酸盐,通过沉淀到沉积物中的硫化物来去除海洋中的亚铁。因此,参与生命进化的硫循环来自于古老的无氧单质硫还原,产生的环境硫化物作为线粒体Fe-S结合到电子传递链中。无氧光合作用可能提供了必要的硫酸盐来促进硫酸盐还原细菌的进化。含氧光合作用的进化提供了多种代谢可能性,包括非光合硫化物氧化、硝化和甲烷化。在氧气存在的情况下,绝缘不良的电线增加(呼吸复合物减少),并且有电子泄漏到分子氧上。电子泄漏导致超氧阴离子(SO)的形成,保留在线粒体基质内。如果不能通过抗氧化防御及时解毒,SO及其衍生的氧化物质可以改变细胞信号传导或攻击细胞结构,导致细胞凋亡。含硫化合物参与氧化应激的产生(在内质网)或(硫醇)抗氧化防御(主要是谷胱甘肽),从而发挥酶活性和基因表达的氧化还原传感作用。导致电子泄漏和氧化应激的硫化合物通过硫醇参与来抵消,作为抗氧化防御者和/或作为氧化还原调节剂或细胞功能,影响生命进化和当代疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Life Evolution on the Sulfur Cycle: From Ancient Elemental Sulfur Reduction and Sulfide Oxidation to the Contemporary Thiol-Redox Challenges
Organismal evolution led to innovations in metabolic pathways, many of which certainly modified the surface chemistry of the Earth. Volcanic activity introduced inorganic com pounds (H 2 , CO 2 , CH 4 , SO 2 , and H 2 S) driving the metabolism of early organisms of the domains archaea and bacteria. In the absence of light, H 2 S and Fe 2+ would have been the major electron donors and the electron acceptors could be either oxidized species such as the sulfurs, sulfate, and elemental sulfur, or carbon dioxide by the fermentation of acetate (forming methane). Elemental sulfur was produced by the reaction between H 2 S and SO 2 , while anoxygenic photosynthesis may have provided the sulfate which removed oceanic ferrous iron by its precipitation as sulfide into sediments. Hence, the sulfur cycle par ticipation in life evolution comes from ancient anoxygenic elemental sulfur reduction generating environmental sulfide incorporated as mitochondrial Fe-S for the electron-transport chains. Anoxygenic photosynthesis may have provided the necessary sulfate to promote the evolution of sulfate-reducing bacteria. The evolution of oxygenic photosyn thesis provided for diverse metabolic possibilities including non-photosynthetic sulfide oxidation, nitrification, and methanotrophy. An increase in badly insulated wires in the presence of oxygen (with reduced respiratory complexes) and there is leakage of electrons on to molecular oxygen. The electron leakage results in the formation of superoxide anion (SO) that remains within the mitochondrial matrix. If not promptly detoxified by anti-oxidative defenses, SO and its derived-oxidative species can alter cell signaling or attack cell structures leading to cell apoptosis. Sulfur-containing compounds participate either in oxidative stress generation (at endoplasmatic reticulum) or in (thiol) antioxidant defenses (mainly glutathione), thus functioning as redox sensing for enzyme activity and gene expression. Sulfur compounds that contributed for electron leakage and oxidative stress have counteractions by thiol participation either as antioxi - dant defensors and/or as redox-modulators or cell functions, influencing life evolution and contemporary diseases.
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