Suzuki H
First Department of Surgery, Nippon Medical School, Tokyo, Japan.
Nihon Ika Daigaku Zasshi. 1991 Apr;58(2):236-42. doi: 10.1272/jnms1923.58.236.
The present study was designed to determine the superoxide production of polymorphonuclear leukocytes (PMN) in endotoxin shock and the antioxidative effect of coenzyme Q10. PMN were collected from rats before and after the intravenous administration of endotoxin. PMN were also collected from healthy humans. Superoxide production of PMN was measured by the cytochrome C method. Lipid peroxide in the liver was examined by the TBA method. Twelve hours after the intravenous administration of 5 mg/kg endotoxin, superoxide production of PMN was 13 times higher than that in the control rats, and the amount of lipid peroxide in the liver was increased. In coenzyme Q10 treated endotoxin shock rats, superoxide production was significantly decreased, and lipid peroxide production in the liver was also inhibited. These findings suggest that endotoxin has a priming effect on the superoxide production of PMN and induces lipid peroxidation. Furthermore coenzyme Q10 has an anti-endotoxin shock effect by inhibiting the superoxide production of PMN and lipid peroxidation in the liver.
本研究旨在确定内毒素休克时多形核白细胞（PMN）的超氧化物生成情况以及辅酶Q10的抗氧化作用。在内毒素静脉注射前后从大鼠体内采集PMN。也从健康人体采集PMN。通过细胞色素C法测量PMN的超氧化物生成。采用TBA法检测肝脏中的脂质过氧化物。静脉注射5mg/kg内毒素12小时后，PMN的超氧化物生成比对照大鼠高13倍，且肝脏中脂质过氧化物的量增加。在辅酶Q10治疗的内毒素休克大鼠中，超氧化物生成显著降低，肝脏中脂质过氧化物的生成也受到抑制。这些发现表明内毒素对PMN的超氧化物生成有启动作用并诱导脂质过氧化。此外，辅酶Q10通过抑制PMN的超氧化物生成和肝脏中的脂质过氧化而具有抗内毒素休克作用。
