Schimke I, Haberland A, Will-Shahab L, Kuttner I, Papies B
Institute of Pathological and Clinical Biochemistry, Humboldt-University, Berlin, GDR.
Biomed Biochim Acta. 1989;48(2-3):S69-72.
In vitro studies have demonstrated that free radicals generated by Fe2+/Vit. C alter the beta-RAS function. SH-oxidation, peroxidation of sarcolemmal lipids and reaction of aldehydes (formed by lipid peroxidation) with the beta-RAS may contribute to this effect. In order to clarify the role of these reactions in respect to their ability to alter the beta-RAS function the time course of SH-oxidation, lipid peroxidation and formation of aldehyde reaction products has been studied. As result it is shown that SH-oxidation is nearly completed within 5 minutes and lipid peroxidation within 30 minutes after exposure to Fe2+/Vit. C. During this time period there was only a very small amount of aldehyde reaction products detectable. Therefore SH-oxidation and/or lipid peroxidation should be responsible for the activity loss of the beta-RAS.
体外研究表明,Fe2+/维生素C产生的自由基会改变β-RAS功能。SH氧化、肌膜脂质过氧化以及醛(由脂质过氧化形成)与β-RAS的反应可能导致这种效应。为了阐明这些反应在改变β-RAS功能方面的作用,研究了SH氧化、脂质过氧化和醛反应产物形成的时间进程。结果表明,暴露于Fe2+/维生素C后,SH氧化在5分钟内几乎完成,脂质过氧化在30分钟内完成。在此时间段内,仅可检测到极少量的醛反应产物。因此,SH氧化和/或脂质过氧化应是导致β-RAS活性丧失的原因。