Sakaguchi S, Kanda N, Hsu C C, Sakaguchi O
Microbiol Immunol. 1981;25(3):229-44. doi: 10.1111/j.1348-0421.1981.tb00026.x.
Lipid peroxide formation and plasma membrane damage in mouse liver following the administration of Salmonella endotoxin were examined. The liver lipoperoxide level was markedly elevated in animals given endotoxin compared with that in the controls, and returned to its normal range after 2 days. On the other hand, superoxide dismutase activity was decreased by 18--48 hr after endotoxin injection, thereafter tending to increase. Glutathione reductase and glutathione peroxidase activities declined in the liver 18 hr after the injection. The endotoxin resulted in much lower lipoperoxide formation in the livers of tolerant mice than in those of the poisoned mice. The lipoperoxide level in endotoxin-poisoned mice after the administration of alpha-tocopherol was lower than that in the controls, and alpha-tocopherol administration prevented completely the membrane protein damage that arose from endotoxin challenge. After glutathione administration the membranes of the poisoned mice also returned to almost the normal disk electrophoretic profile. These results suggest that lipid peroxide formation in the liver plasma membrane caused by free radicals might occur in a tissue ischemic state in endotoxicosis.
研究了给予沙门氏菌内毒素后小鼠肝脏中脂质过氧化物的形成及质膜损伤情况。与对照组相比,给予内毒素的动物肝脏脂质过氧化物水平显著升高,并在2天后恢复至正常范围。另一方面,超氧化物歧化酶活性在内毒素注射后18 - 48小时降低,此后趋于升高。注射后18小时,肝脏中的谷胱甘肽还原酶和谷胱甘肽过氧化物酶活性下降。内毒素导致耐受小鼠肝脏中脂质过氧化物的形成比中毒小鼠的要低得多。给予α-生育酚后,内毒素中毒小鼠的脂质过氧化物水平低于对照组,并且给予α-生育酚完全防止了内毒素攻击引起的膜蛋白损伤。给予谷胱甘肽后,中毒小鼠的膜也几乎恢复到正常的圆盘电泳图谱。这些结果表明,内毒素血症中组织缺血状态下可能会发生由自由基引起的肝质膜脂质过氧化物形成。