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作 者:唐庆娟[1] 陶凯忠[1] 胡淼淼[1] 徐胜[1] 徐建平[1] 崔瑞耀[2] 蒋春雷[1]
机构地区:[1]第二军医大学海军医学系航海医学教研室,上海200433 [2]青岛大学医学院病理生理学教研室,山东青岛266021
出 处:《中国行为医学科学》2003年第5期500-500,519,共2页Chinese Journal of Behavioral Medical Science
摘 要:目的 观察 72h睡眠剥夺大鼠的氧化应激状态。方法 参照Everson等的方法 ,将SD大鼠予以 72h剥夺睡眠处理后 ,断头取血 ,比色法测定血浆丙二醛 (MDA)和还原型谷胱甘肽 (GSH)的含量以及谷胱甘肽过氧化物酶 (GSH Px)、谷胱甘肽还原酶 (GSH R)和超氧化物岐化酶 (SOD)的活性。结果 与对照组相比 ,睡眠剥夺大鼠血浆MDA的含量增高 ,GSH含量降低 ,GSH Px和GSH R活性降低 ,SOD活性有降低趋势。结论 72h睡眠剥夺大鼠处于氧化应激状态 ,氧化应激可能是睡眠剥夺引起病理变化的机制之一。Objective To observe oxidative stress of rats induced by 72h sleep deprivation. Methods Using a modified method of Everson et al, male SD rats were sleep deprived for 72h, and contents of plasma malondialhyde (MDA) and glutathione (GSH) and activity of plasma glutathione peroxidase (GSH-Px), glutathione reductase (GSH-R) and superoxide dismutase (SOD) were measured. Results Compared with the control group, plasma MDA of experimental rats increased, and GSH decreased. After 72h sleep deprivation, both GSH-Px and GSH-R activity were reduced, and SOD activity showed a tendency to decrease. Conclusion 72h sleep deprivation promotes oxidative stress, which may be a mechanism mediating injuries by sleep deprivation.
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