Sevanian A, Muakkassah-Kelly S F, Montestruque S
Arch Biochem Biophys. 1983 Jun;223(2):441-52. doi: 10.1016/0003-9861(83)90608-2.
The relationship between release of membrane lipid peroxidation products and phospholipase action was examined. Rat liver microsomes and phosphatidylcholine liposome-phospholipase A2 preparations were subjected to iron ascorbate-induced lipid peroxidation. Peroxidation products were characterized by measurement of malondialdehyde and lipid peroxides. Experiments were designed to demonstrate phospholipase dependent removal of peroxidation products origination in the membrane. Increased lysophosphatidylcholine formation was evident following lipid peroxidation in phospholipase A2-containing liposomes which was inhibited by p-bromophenacyl bromide and mepacrine. Lipoxygenase-dependent oxygen consumption, as well as peroxide transfer from microsomes to the incubation medium, was largely dependent on phospholipase and could be diminished by phospholipase inhibitors. Furthermore, lipid hydroperoxides formed by subjecting phosphatidylcholine liposomes to iron ascorbate-induced peroxidation, or those present in aged liposomes, were effectively reduced by glutathione peroxidase when phospholipase A2 was present in the assay. Low level glutathione peroxidase activity was observed in the absence of phospholipase A2.
研究了膜脂质过氧化产物释放与磷脂酶作用之间的关系。将大鼠肝微粒体和磷脂酰胆碱脂质体 - 磷脂酶A2制剂进行抗坏血酸铁诱导的脂质过氧化。通过测量丙二醛和脂质过氧化物来表征过氧化产物。设计实验以证明磷脂酶依赖性去除膜中产生的过氧化产物。在含磷脂酶A2的脂质体中进行脂质过氧化后，溶血磷脂酰胆碱形成增加，这被对溴苯甲酰溴和米帕林抑制。脂氧合酶依赖性耗氧量以及过氧化物从微粒体向孵育介质的转移在很大程度上依赖于磷脂酶，并且可以被磷脂酶抑制剂减少。此外，当测定中存在磷脂酶A2时，通过使磷脂酰胆碱脂质体进行抗坏血酸铁诱导的过氧化形成的脂质氢过氧化物或老化脂质体中存在的脂质氢过氧化物被谷胱甘肽过氧化物酶有效还原。在没有磷脂酶A2的情况下观察到低水平的谷胱甘肽过氧化物酶活性。
