Dudnik L B, Bilenko M V, Alesenko A V, Slesareva L D, Burlakova E B
Biull Eksp Biol Med. 1980 May;89(5):556-8.
Lipid peroxidation (hydroperoxides and antioxidant activity) and lipid composition in liver homogenates and in its mitochondrial, microsomal and nuclear fractions were studied after 15--120 minutes of liver warm ischemia. Pronounced enhancement of lipid peroxidation during ischemia was seen in all subcellular fractions, particularly in the mitochondrial one. The results are consistent with low resistance of the liver and specifically its mitochondria to ischemia. Activation of lipid peroxidation corresponded with changes in the lipid composition. Decrease in the level of total and readily oxidizable lipids (cardiolipin) and accumulation of poorly oxidizable phospholipids (sphingomyelin) and highly toxic lysophosphatides were recorded. The evidence obtained suggests a role for lipid peroxidation in the pathogenesis of ischemic injuries to the liver.
在肝脏热缺血15 - 120分钟后，对肝脏匀浆及其线粒体、微粒体和细胞核部分的脂质过氧化（氢过氧化物和抗氧化活性）及脂质组成进行了研究。在所有亚细胞部分，尤其是线粒体部分，缺血期间脂质过氧化明显增强。结果表明肝脏，特别是其线粒体对缺血的耐受性较低。脂质过氧化的激活与脂质组成的变化相对应。记录到总脂质和易氧化脂质（心磷脂）水平降低，难氧化磷脂（鞘磷脂）和高毒性溶血磷脂积累。所获得的证据表明脂质过氧化在肝脏缺血性损伤的发病机制中起作用。
