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首页> 外文期刊>Biological chemistry >Irreversible Thiol Oxidation in Carbonic Anhydrase III: Protection by S-Glutathiolation and Detection in Aging Rats
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Irreversible Thiol Oxidation in Carbonic Anhydrase III: Protection by S-Glutathiolation and Detection in Aging Rats

机译：碳酸酐酶III中不可逆的硫醇氧化：衰老大鼠中S-谷硫醇的保护和检测

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摘要

Proteins with reactive sulfhydryls are central to many important metabolic reactions and also contribute to a variety of signal transduction systems. In this report, we examine the mechanisms of oxidative damage to the two reactive sulfhydryls of carbonic anhydrase III. Hydrogen peroxide (H_2O_2), peroxy radicals, oxidized forms, primarily cysteine sulfinic acid or cysteic acid, of carbonic anhydrase III if glutathione (GSH) was not present. When GSH was approximately equimolar to protein thiols, irreversible oxidation was prevented. H_2O_2 and peroxyl radicals both generated S-glutathiolated carbonic anhydrase III via partially oxidized protein sulfhydryl intermediates, while HOCI did not cause S-glutathiolation. Thus, oxidative damage from H_2O_2 or AAPH was prevented by protein S-glutathiolation, while a direct reaction between GSH and oxidant likely prevents HOCI-mediated protein damage. In cultured rat hepatocytes, carbonic anhydrase III was rapidly S-glutathiolated by menadione. When hepatocyte glutathione was depleted, menadione instead caused irreversible oxidation. We hypothesized that normal depletion of glutathione in aged animals might also lead to an increase in irreversible oxidation. Indeed, both total protein extracts and carbonic anhydrase III contained significantly more cysteine sulfinic acid in older rats compared to young animals. These experiments show that, in the absence of sufficient SGH, oxidation reactions lead to irreversible protein sulfhydryl damage in purified proteins, cellular systems, and whole animals.
机译：具有反应性巯基的蛋白质对于许多重要的新陈代谢反应至关重要，也有助于多种信号转导系统。在这份报告中，我们研究了氧化作用对碳酸酐酶III的两个反应性巯基的损害。如果不存在谷胱甘肽（GSH），则碳酸酐酶III的过氧化氢（H_2O_2），过氧自由基，氧化形式（主要是半胱氨酸亚磺酸或半胱氨酸）会被氧化。当GSH与蛋白质硫醇近似等摩尔时，可以防止不可逆的氧化。 H_2O_2和过氧自由基均通过部分氧化的蛋白质巯基中间体生成S-戊二硫代碳酸酐酶III，而HOCI不会引起S-戊二硫代化。因此，蛋白S-谷氨硫醇化可防止H_2O_2或AAPH的氧化损伤，而GSH与氧化剂之间的直接反应则可能阻止HOCI介导的蛋白损伤。在培养的大鼠肝细胞中，甲萘醌将碳酸酐酶III迅速S-谷氨酰胺化。当肝细胞谷胱甘肽耗尽时，甲萘醌会引起不可逆的氧化。我们假设正常衰老动物体内的谷胱甘肽消耗也可能导致不可逆氧化增加。确实，与年幼动物相比，年长大鼠的总蛋白质提取物和碳酸酐酶III都含有明显更多的半胱氨酸亚磺酸。这些实验表明，在没有足够的SGH的情况下，氧化反应会导致纯化的蛋白质，细胞系统和整个动物体内不可逆的蛋白质巯基损坏。

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