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目的:探讨弱精症发病的分子机制。方法:收集113例弱精症患者和58例年龄相仿的健康志愿者正常精液样本,分离精子、精浆,分别检测其氧化损伤状态。结果:弱精症患者组的精浆样本中,总抗氧化能力(T-AOC),铜锌-超氧化物歧化酶(SOD-1),总超氧化物歧化酶(T-SOD),还原型谷胱甘肽(GSH)的结果均低于正常组,但是谷胱甘肽-S-转移酶(GST)活力显著性高于正常组;精子裂解液测定结果显示,弱精症患者的SOD-1和T-SOD的活力显著性低于正常组,而GST活力两组基本相当。结论:弱精症患者精液中存在的由于DJ-1低表达而引起的氧化应激损伤,是其可能的发病分子机制之一。
Objective: To explore the molecular mechanism of asthenospermia. Methods: The normal semen samples of 113 patients with asthenospermia and 58 healthy volunteers of the same age were collected. Sperm and seminal plasma were separated and their oxidative damage status was examined. Results: In seminal plasma samples from patients with asthenospermia, the total antioxidant capacity (T-AOC), copper-zinc-superoxide dismutase (SOD-1) and total superoxide dismutase (T-SOD) The results of prototype GSH were lower than those of normal group, but the activity of glutathione-S-transferase (GST) was significantly higher than that of normal group. The results of sperm lysis showed that SOD -1 and T-SOD activity was significantly lower than the normal group, while the GST activity of the two groups were basically the same. Conclusion: The oxidative stress injury caused by the low expression of DJ-1 in seminal fluid of asthenozoospermic patients is one of the possible molecular pathogenesis.