儿茶酚胺类神经递质介导的活性氧损伤作用的初步研究

A Preliminary Study of Catecholamine Mediated Oxidative Damage

目的:探讨儿茶酚胺类神经递质对机体损伤的机制。方法:观察儿茶酚胺自氧化对红细胞的过氧化作用,并以乙肝病毒表面抗体为代表靶,观察儿茶酚胺自氧化对抗体活性的影响。结果:肾上腺素可以显著地增加红细胞脂质过氧化的水平,增加比为19%(P<0.05),而去甲肾上腺素的作用不显著。肾上腺素和去甲肾上腺素均可以显著地增加酶联反应的产物(P<0.05)。产物的吸光度增加(492nm),标本/阴性对照比值(P/N)增加4倍以上。联合应用超氧化物歧化酶和过氧化氢酶几乎完全抑制儿茶酚胺对抗体的激活作用。结论:肾上腺素和去甲肾上腺素通过自氧化所产生的氧自由基攻击抗体很可能是造成抗体活性增强的原因。

Aim： To study the mechanism of catecholamine mediated oxidative damage which is in psychological pressure. Methods： The catecholamine mediated oxidative damage of erythrocyte often produced membrane was investigated by TBA method, as well as the influence of catecholamine on antibody reactivity. Results： Epinephrine significantly increased the lipid peroxidation of erythrocyte membrane up to 19% （P〈 0.05）, however, noradrenalin had little effect. Both epinephrine and noradrenalin significantly increased the antibody reactivities, the products of antibody measured by 492 nm optical absorbance were increased. P/N ratio increased up to 4 times. Combination with SOD and catalase almost completely inhibited the effects. Conclusion： Our results suggest that both epinephrine and noradrenalin are meaningful for unders able to produce reactive oxygen which may induce higher reactivity of antibody. This study is tanding the mechanism of autoimmunological diseases under psychological stress.