钙对脂质过氧化的双相效应。
The biphasic effect of calcium on lipid peroxidation.
作者信息
Babizhayev M A
机构信息
Moscow Helmholtz Research Institute of Eye Diseases, USSR.
出版信息
Arch Biochem Biophys. 1988 Nov 1;266(2):446-51. doi: 10.1016/0003-9861(88)90276-7.
Mechanisms underlying Ca2+ effects on lipid peroxidation (LPO) induced in liposomes (from egg yolk lecithin) and ufasomes (from linolenic acid and methyl linolenate) with the aid of an O2-(.) -generating system (Fe2+ + ascorbate) were studied. It was shown that stimulation of LPO by low Ca2+ concentrations (10(-6)-10(-5)M) was due to its ability to release Fe2+ ions bound to negatively charged (phosphate or carboxylic) lipid groups (of lecithin or linolenic acid), thus increasing the concentration of catalytically active Fe2+. The inhibitory effect of high Ca2+ concentrations was caused by its interaction with superoxide anion radicals and was not observed in LPO systems independent of O2- generation (e.g., Fe2+ + cumol hydroperoxide).
研究了在借助超氧阴离子（·O₂⁻）生成系统（Fe²⁺ + 抗坏血酸）的情况下，Ca²⁺对脂质体（由蛋黄卵磷脂制成）和不饱和脂质体（由亚麻酸和亚麻酸甲酯制成）中诱导的脂质过氧化（LPO）的影响机制。结果表明，低Ca²⁺浓度（10⁻⁶ - 10⁻⁵M）对LPO的刺激作用是由于其能够释放与带负电荷的（磷脂或羧基）脂质基团（卵磷脂或亚麻酸的）结合的Fe²⁺离子，从而增加了具有催化活性的Fe²⁺的浓度。高Ca²⁺浓度的抑制作用是由其与超氧阴离子自由基的相互作用引起的，并且在与超氧阴离子生成无关的LPO系统（例如，Fe²⁺ + 氢过氧化茴香醚）中未观察到这种抑制作用。
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