中国地方病学杂志
中國地方病學雜誌
중국지방병학잡지
CHINESE JOURNAL OF ENDEMIOLOGY
2009年
3期
332-334
,共3页
王宇%裴俊瑞%李兴洲%高琳%闫丽佳%李奇%侯杰%周令望%张立君%李少臣%刘明法%王铜
王宇%裴俊瑞%李興洲%高琳%閆麗佳%李奇%侯傑%週令望%張立君%李少臣%劉明法%王銅
왕우%배준서%리흥주%고림%염려가%리기%후걸%주령망%장립군%리소신%류명법%왕동
克山病%氧化性应激%硒%谷胱甘肽过氧化物酶
剋山病%氧化性應激%硒%穀胱甘肽過氧化物酶
극산병%양화성응격%서%곡광감태과양화물매
Keshan disease%Oxidative stress%Selenium%Glutathione peroxidase
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.
目的 探討剋山病患者體內抗氧化水平與剋山病心肌損傷的關繫,分析其可能的髮病機製.方法 2005和2006年期間,在黑龍江省剋山病重病區富裕縣永進村和新髮村、尚誌市扶安村、五大連池市星火村選擇慢型、潛在型剋山病患者41名作為病例組,61名健康人作為病區對照組;在非病區望奎縣廂蘭三村選取48名健康人作為非病區對照組,分彆採集清晨空腹外週靜脈血檢測全血硒水平、全血穀胱甘肽過氧化物酶(GSH-Px)活力、血漿總超氧化物歧化酶(T-SOD)活力及血漿丙二醛(MDA)水平.結果 病例組血硒水平[(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]顯著低于病區對照組[(41.24±13.57)μg/L、(118.57±25.49)U/L、(104.82±13.56)×103 U/L]和非病區對照組[(48.33±16.51)μg/L、(155.00±24.01)U/L、(108.48±12.73)×103 U/L],組間比較差異有統計學意義(P均<0.05);病例組MDA水平[(7.12±1.37)μmol/L]高于病區對照組[(5.36±1.18)μmol/L]和非病區對照組[(5.22±0.83)μmol/L],組間比較差異有統計學意義(P均<0.05);病區對照組血硒水平、GSH-Px活力低于非病區對照組(P<0.05),組間比較差異均有統計學意義(P<0.05).結論 剋山病病人體內存在硒缺乏所緻的抗氧化能力降低,氧化損傷增彊.氧化應激障礙可能與剋山病的心肌損傷有一定的關繫.
목적 탐토극산병환자체내항양화수평여극산병심기손상적관계,분석기가능적발병궤제.방법 2005화2006년기간,재흑룡강성극산병중병구부유현영진촌화신발촌、상지시부안촌、오대련지시성화촌선택만형、잠재형극산병환자41명작위병례조,61명건강인작위병구대조조;재비병구망규현상란삼촌선취48명건강인작위비병구대조조,분별채집청신공복외주정맥혈검측전혈서수평、전혈곡광감태과양화물매(GSH-Px)활력、혈장총초양화물기화매(T-SOD)활력급혈장병이철(MDA)수평.결과 병례조혈서수평[(34.80±13.30)μg/L]、GSH-Px활력[(104.10±34.19)U/L]、T-SOD활력[(92.16±17.98)×103 U/L]현저저우병구대조조[(41.24±13.57)μg/L、(118.57±25.49)U/L、(104.82±13.56)×103 U/L]화비병구대조조[(48.33±16.51)μg/L、(155.00±24.01)U/L、(108.48±12.73)×103 U/L],조간비교차이유통계학의의(P균<0.05);병례조MDA수평[(7.12±1.37)μmol/L]고우병구대조조[(5.36±1.18)μmol/L]화비병구대조조[(5.22±0.83)μmol/L],조간비교차이유통계학의의(P균<0.05);병구대조조혈서수평、GSH-Px활력저우비병구대조조(P<0.05),조간비교차이균유통계학의의(P<0.05).결론 극산병병인체내존재서결핍소치적항양화능력강저,양화손상증강.양화응격장애가능여극산병적심기손상유일정적관계.
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.
