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首页> 外文期刊>Life sciences >PROTECTION BY PYRUVATE AGAINST INHIBITION OF NA+,K+-ATPASE BY A FREE RADICAL GENERATING SYSTEM CONTAINING T-BUTYLHYDROPEROXIDE
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PROTECTION BY PYRUVATE AGAINST INHIBITION OF NA+,K+-ATPASE BY A FREE RADICAL GENERATING SYSTEM CONTAINING T-BUTYLHYDROPEROXIDE

机译：丙酮酸对包含叔丁基过氧化氢的自由基生成系统的NA +，K + -ATPase抑制作用的保护

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Global tissue damage due to oxygen-derived free radicals has been implicated in several pathological processes including exposure to ionizing radiation, and postischemic reperfusion of the heart or kidney. Recently pyruvate, a hydroperoxide scavenger, has been shown to protect against functional damage during postischemic reperfusion of the heart and in acute renal failure. In the present study, pyruvate was found to protect against inactivation of partially purified guinea pig renal and rat cardiac Na+,K+-ATPase which occurred when microsomal membranes were assayed for 1 hr at 37 degrees C (pH 7.5) in the presence of a free radical generating system (FRGS) containing 0.3 mM t-butylhydroperoxide and horseradish peroxidase. The presence of the FRG system inhibited the guinea pig renal Na+,K+-ATPase activity by 48.2+/-4.8% (N=10, P<.05) and the presence of 0.2 to 20 mM pyruvate partially protected the Na+,K+-ATPase. At 5 mM pyruvate Na+,K+-ATPase was inhibited by only 18.8+/-2.5% (N=10, P<.05) but increasing the pyruvate concentration gave no further protection. Equimolar concentrations of glucose, mannitol or lactate were without effect. The protection appeared to require an alpha-keto acid since alpha- but not beta-ketoglutarate was also effective and the mechanism is most probably the scavenging of t-BHO2. The results of the present study therefore support the hypothesis that, if free radical damage to native Na+,K+-ATPase does contribute to global tissue injury in certain pathological processes, pyruvate, in addition to being a powerful metabolic effector of recovery, may also protect against oxidative damage. [References: 36]
机译：由氧衍生的自由基引起的整体组织损伤与多种病理过程有关，包括暴露于电离辐射以及心脏或肾脏的缺血性再灌注。最近，丙酮酸（一种氢过氧化物清除剂）已显示出在心脏缺血再灌注期间和急性肾功能衰竭中可防止功能受损。在本研究中，发现丙酮酸可防止部分纯化的豚鼠肾和大鼠心脏Na +，K + -ATPase失活，这种失活是在游离液存在下于37摄氏度（pH 7.5）下测定微粒体膜1小时时发生的。自由基生成系统（FRGS），其中包含0.3 mM叔丁基过氧化氢和辣根过氧化物酶。 FRG系统的存在抑制了豚鼠肾Na +，K + -ATPase活性48.2 +/- 4.8％（N = 10，P <.05），而0.2至20 mM丙酮酸的存在部分保护了Na +，K +- ATP酶。在5 mM丙酮酸下，Na +，K + -ATPase仅被抑制了18.8 +/- 2.5％（N = 10，P <.05），但是增加丙酮酸浓度并没有提供进一步的保护。葡萄糖，甘露醇或乳酸的等摩尔浓度无效。这种保护似乎需要α-酮酸，因为α-酮戊二酸也很有效，但其作用机制很可能是清除t-BHO2。因此，本研究的结果支持以下假说：如果自由基对天然Na +，K + -ATPase的破坏确实在某些病理过程中造成了整体组织损伤，那么丙酮酸除了是恢复的强大代谢效应因子外，还可以保护防止氧化损伤。 [参考：36]

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