摘要
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。
The damage of oxygen-derived free radicals to hepatic cells and subcellular organelles during endotoxic shock was studied. At 30 minutes after shock, although the contents of malondialdehyde (MDA) in hepatic tissue had no change (P>0.05), the contents of MDA in hepatic mitochondria and lysosomc suspensions elevated (P<0.05). At the same time the activities of supcroxide dismutasc (SOD) in hepatic tissue, mitochondria and lysosomc suspensions increased (P<0.05). At 2 hours after shock the contents of MDA in all hepatic tissue, mitochondria and lysosornc suspensions elevated (P<0.01-0.001) and the activities of SOD in hepatic mitochondria and lysosomc suspensions began to decrease (P<0.05). The activities of SOD in hepatic tissue, mitochondria and lysosome suspensions were depressed severely (P<0.01-0.001) at 4 hours after shock. These data showed that oxygen-derived free radicals resulted in the lipid pcroxidation injury of hepatic cells and organelles, furthermore, the damage of hepatic subccllular organcIles such as mitochondria and lysosome might occur much earlier than the damage of hepatic tissue
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1990年第1期28-31,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金
关键词
休克
内毒素
自由基
脂质过氧化
Shock, septic
Malondialdebyde
Superoxide dismutase
Mitochondria
Lysosomes
