内毒素对大鼠脑线粒体的损伤及与氧自由基的关系

The damage of rat brain mitochondria induced by endotoxin and its relation to oxygen free radical metabolism

本文观察了在较低剂量(2mg/kg)E.Coli内毒素纯制剂腹腔注射后,大鼠脑组织线粒体的过氧化脂质和与氧自由基代谢及线粒体完整性密切相关的酶的活性变化。结果表明,在内毒素注射后14小时鼠脑线粒体LPO较对照组升高21%(P<0.01),SOD、GSH-Px、SDH活性均明显下降,分别较对照组低18%、30%、22.3%(均P<0.01)。24小时开始恢复,即LPO下降,其它酶学指标回升。48小时各项指标均基本回到对照组水平。电镜观察证实内毒素注射后14小时脑组织线粒体肿胀。上述结果提示:这种剂量的内毒素造成了脑组织的可逆性损害。自由基清除能力降低,膜脂质过氧化作用增强是引起大鼠脑线粒体损害的重要原因。

The study was undertaken to determine whether low dose of endotoxin could induce rat brain damage, and its relation to the metabolism of oxygen free radicals. Male Wistar rats were treated with E. Coli endotoxin intraperitoneally (2 mg/kg body wt). Fourteen hours later, the lipoperoxide level was markedly elevated in animals given endotoxin compared with that in the controls (5.0±1.0 vs 3.9±0.7, P<0.01). On the other hand, a very significant reduction of activities of succinic dehydrogenase, superoxide dismutase, and glutathione peroxidase were observed (respectely P<0.01). Under electron microscope, the swelling of mitochondria was seen without fragmentation of other subcellular organelle. Data showed signs of recovery after 24 hr and returned to their normal ranges after 2 days. These results suggest that endotoxin at the dosage of 2 mg/kg gives rise to the accumulation of lipoperoxide in rat brain mitochondria by activation of producing system and impairment of scavenging system of oxygen free radicals.