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首页> 外文期刊>Life sciences >Genistein abrogates pre-hemolytic and oxidative stress damage induced by 2,2'-Azobis (Amidinopropane).
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Genistein abrogates pre-hemolytic and oxidative stress damage induced by 2,2'-Azobis (Amidinopropane).

机译：金雀异黄素消除了由2,2'-Azobis（A基丙烷）引起的溶血前和氧化应激损伤。

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摘要

The pre-hemolytic mechanism induced by free radicals initiated from water-soluble 2,2'-azobis (2-amidinopropane) hydrochloride (AAPH) and its reversal by genistein was investigated in human erythrocytes. The time course of K+ efflux compared to the occurrence of hemolysis suggests that AAPH-induced hemolysis occurs indirectly via pore formation and band 3 oxidation as expected. However, genistein inhibited hemolysis, LDH release and membrane protein oxidation but not K+ efflux. This indicated that erythrocyte protein oxidation possibly in the hydrophobic core plays a significant role in the membrane pre-hemolytic damage. Chemiluminescence (CL) analysis carried out in non-lysed erythrocytes treated with AAPH showed a dramatic increase in CL indicating both reduced levels of antioxidants and increased membrane lipid peroxide. The V0 value was also increased up to 6 times, denoting a high degree of membrane peroxidation very early in erythrocyte membrane damage. The whole process was inhibited by genistein in a dose-dependent manner. These results indicate that the genistein inhibited both hemolysis and pre-hemolytic damage and also hindered membrane lipid peroxide formation and protein oxidation. In addition, it is suggested that pre-hemolytic damage is mediated mainly by the oxidation of both phospholipid and protein located in the deeper hydrophobic region of the membrane.
机译：在人类红细胞中研究了由水溶性2,2'-偶氮双（2-ami基丙烷）盐酸盐（AAPH）引发的自由基诱导的自由基的预溶血机理及其通过染料木黄酮逆转的机理。与溶血的发生相比，钾离子外流的时间过程表明，AAPH诱导的溶血通过孔隙形成和谱带3氧化而间接发生。然而，金雀异黄素抑制溶血，LDH释放和膜蛋白氧化，但不抑制K +流出。这表明可能在疏水核心中的红细胞蛋白氧化在膜预溶血性损伤中起重要作用。在用AAPH处理的未裂解的红细胞中进行的化学发光（CL）分析显示，CL显着增加，表明抗氧化剂含量降低和膜脂质过氧化物含量增加。 V0值也增加了多达6倍，这表明在红细胞膜损伤的早期非常高的膜过氧化程度。染料木黄酮以剂量依赖的方式抑制了整个过程。这些结果表明金雀异黄素抑制溶血和溶血前的损害，也阻碍了膜脂质过氧化物的形成和蛋白质的氧化。另外，建议溶血前损伤主要由位于膜的更深疏水区域的磷脂和蛋白质的氧化介导。

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