Anzai K, Ogawa K, Goto Y, Senzaki Y, Ozawa T, Yamamoto H
Bioregulation Research Group, National Institute of Radiological Sciences, Japan.
Antioxid Redox Signal. 1999 Fall;1(3):339-47. doi: 10.1089/ars.1999.1.3-339.
Peroxidation-dependent change in the permeability of lipid bilayers was mesaured by using artificial membrane systems, that is, planar lipid bilayers and liposomes. The unsaturated fatty acyl chains of phospholipids in small unilamellar vesicles were peroxidized time-dependently by the hydroxyl radical chemically generated by the reaction of H2O2 and Cu(en)2. In contrast, at the same hydroxyl radical concentration and time ranges, no ionic current through the planar lipid bilayers and no release of K+ from the liposomes were observed. These findings indicate that accumulation of lipid peroxide within lipid bilayers is not responsible for the permeability increase that is often observed in biomembranes exposed to oxidative stresses. Higher concentration of the hydroxyl radical caused break-down of the planar lipid bilayers composed of the mixture (7:3) of phosphatidylethanolamine (PE) and phosphatidylcholine (PC). The bilayer containing 100% PE at least at one leaflet of the bilayer (facing the hydroxyl radical-generating solution) was not broken-down by the application of the hydroxyl radical, suggesting that PE stabilizes the planar lipid bilayer against the attack of the hydroxyl radical.
通过使用人工膜系统，即平面脂质双层和脂质体，来测量脂质双层膜通透性的过氧化依赖性变化。小单层囊泡中磷脂的不饱和脂肪酰链会被H2O2与Cu(en)2反应化学产生的羟基自由基随时间进行过氧化。相比之下，在相同的羟基自由基浓度和时间范围内，未观察到通过平面脂质双层的离子电流，脂质体中也没有K+释放。这些发现表明，脂质双层内脂质过氧化物的积累并非生物膜在氧化应激下常见的通透性增加的原因。较高浓度的羟基自由基导致由磷脂酰乙醇胺（PE）和磷脂酰胆碱（PC）的混合物（7:3）组成的平面脂质双层破裂。至少在双层的一个小叶（面向产生羟基自由基的溶液）含有100% PE的双层不会因施加羟基自由基而破裂，这表明PE可稳定平面脂质双层抵抗羟基自由基的攻击。
