克山病患者抗氧化能力测定

目的 探讨克山病患者体内抗氧化水平与克山病心肌损伤的关系,分析其可能的发病机制.方法 2005和2006年期间,在黑龙江省克山病重病区富裕县永进村和新发村、尚志市扶安村、五大连池市星火村选择慢型、潜在型克山病患者41名作为病例组,61名健康人作为病区对照组;在非病区望奎县厢兰三村选取48名健康人作为非病区对照组,分别采集清晨空腹外周静脉血检测全血硒水平、全血谷胱甘肽过氧化物酶(GSH-Px)活力、血浆总超氧化物歧化酶(T-SOD)活力及血浆丙二醛(MDA)水平.结果 病例组血硒水平(34.80±13.30)μg/L]、GSH-Px活力(104.10±34.19)U/L]、T-SOD活力(92.16±17.98)×103 U/L]显著低于病区对照组(41.24±13.57)μg/L、(118.57±25.49)U/L、(104.82±13.56)×103 U/L]和非病区对照组(48.33±16.51)μg/L、(155.00±24.01)U/L、(108.48±12.73)×103 U/L],组间比较差异有统计学意义(P均<0.05);病例组MDA水平(7.12±1.37)μmol/L]高于病区对照组(5.36±1.18)μmol/L]和非病区对照组(5.22±0.83)μmol/L],组间比较差异有统计学意义(P均<0.05);病区对照组血硒水平、GSH-Px活力低于非病区对照组(P<0.05),组间比较差异均有统计学意义(P<0.05).结论 克山病病人体内存在硒缺乏所致的抗氧化能力降低,氧化损伤增强.氧化应激障碍可能与克山病的心肌损伤有一定的关系.

An observation on antioxidant capacity of Keshan disease patients

Objective To explore the relationship between myocardial damage and antioxidant capacity in vivo of Keshan disease patients and to analyze the possible pathogenesis. Methods In the period from 2005 to 2006, 41 chronic and latent Keshan disease cases were chosen as the case group from such serious endemic areas as Yongjin Village, Xinfa Village of Fuyu County, Fuan Village of Shangzhi County, Xinghuo Village of Wudalianchi County, 61 healthy people from the same area as internal controls, 48 healthy people from Xianglansan Village of Wangkui County, an un-endemic area, as external control. Fasting peripheral venous blood was collected from all the people. And blood selenium, glutathione peroxidase(GSH-Px) and suporoxide dismutase.(T-SOD) activities, malondialdehyde (MDA) levels were examined. Results Blood selenium level of the patient group (34.80±13.30) μg/L], GSH-Px(104.10±34.19)U/L]and T-SOD(92.16±17.98)×103 U/L]actives were significantly lower than the internal control group (41.24±13.57)μg/L, (118.57±25.49)U/L, (104.82±13.56)×103 U/L]and the external control group (48.33±16.51)μg/L, (155.00±24.01)U/L, (108.48±12.73)×103 U/L], respectively, with a statistically significant difference(all P < 0.05). MDA level of the patient group(7.12± 1.37)μmol/L]was higher than that in the internal control group(5.36±1.18)μmol/L]and the external control group(5.22±0.83)μmol/L]with a statistically significant differences(both P < 0.05). The blood selenium level, GSH-Px activity of internal control group was resoectively lower than that in the external control group, the differences being statistically significant(beth P < 0.05). Conclusions Selenium deficiency may lead to reduced antioxidant capacity and enhanced oxidative damage in Keshan disease patients in vivo. There may be a certain relationship between oxidative stress disorder and myocardial damage of Keshan disease.