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本文探讨氧衍生的自由基在内毒素休克时对肝脏细胞和亚细胞的损伤作用。给大鼠静注内毒素(3mg/kg体重)0.5小时后,尽管肝组织MDA没有明显升高(P>0.05),但线粒体和溶酶体悬液中MDA以及肝组织、线粒体、溶酶体SOD较对照已明显升高(P<0.05)。休克后2小时,肝组织、线粒体、溶酶体MDA均显著升高(P<0.01～0.001),以后升高更甚(P<0.001)。线粒体、溶酶体SOD在休克后2小时明显下降(P<0.05),休克后4小时肝组织和亚细胞器SOD均明显受抑(P<0.01～0.001)。血浆,溶血液MDA、SOD和溶酶体酶在休克后均有程度不同的改变。实验结果表明氧衍生的自由基在内毒素休克时引起肝细胞和线粒体、溶酶体等亚细胞器的脂质过氧化损伤,而亚细胞器的损伤似乎早于组织损伤。
This article explores the role of oxygen-derived free radicals in damaging liver cells and subcellular cells during endotoxic shock. After intravenous injection of endotoxin (3mg / kg body weight) for 0.5h, the content of malondialdehyde (MDA) in the mitochondria and lysosome suspension, liver tissue, mitochondria, lysosome SOD was significantly higher than the control (P <0.05). At 2 hours after shock, the levels of MDA in liver tissue, mitochondria and lysosome increased significantly (P <0.01 ~ 0.001), and then increased even more (P <0.001). Mitochondria and lysosomal SOD decreased significantly 2 hours after shock (P <0.05), and were significantly inhibited at 4 hours after shock (P <0.01-0.001). Plasma, hemolysate MDA, SOD and lysosomal enzymes in shock after varying degrees of change. The experimental results show that oxygen-derived free radicals cause lipid peroxidation damage in liver cells and mitochondria, lysosomes and other subcellular organelles during endotoxic shock, whereas subcellular organelles appear to be earlier damaged than tissue damage.