中文摘要：

[目的]了解燃煤砷暴露人群外周血中铜锌超氧化物歧化酶（Cu/Zn-SOD）和谷胱甘肽过氧化物酶（GSH-Px）1转录表达与酶活力的关系,探讨其在燃煤型砷中毒肝损伤发生发展中的作用。[方法]选择燃煤型砷中毒病区133例砷暴露者为砷暴露组（包括病区非病例组25例和病例组108例）,将病例组分为无明显肝病组（38例）和肝病组（分为轻度肝病组43例和中重度肝病组27例）;在非砷暴露村选择34例经健康体检无异常的居民作为对照组。采集上述观察对象的外周血,采用实时荧光定量PCR法检测Cu/Zn-SOD mRNA和GSH-Px1 mRNA表达,化学法检测SOD、Cu/Zn-SOD和GSH-Px活力。[结果]与对照组比较,肝病组Cu/Zn-SOD mRNA和GSH-Px1 mRNA表达量均明显升高（P〈0.05或P〈0.01）;与病区非病例组比较,肝病组Cu/Zn-SOD mRNA表达量明显升高（P〈0.05）;各病例组间比较差异无统计学意义。与对照组和病区非病例组比较,肝病组SOD、Cu/Zn-SOD和GSH-Px活力均明显降低（P〈0.05或P〈0.01）;与无明显肝病组比较,轻度肝病组SOD和Cu/Zn-SOD活力明显下降（P〈0.05）,而中重度肝病组三种酶活力均明显下降（P〈0.05或P〈0.01）;与轻度肝病组比较,中重度肝病组SOD活力明显降低（P〈0.05）。Cu/Zn-SOD和GSH-Px1转录表达与肝损伤程度呈正相关（P〈0.01）,酶活力与肝损伤程度呈负相关（P〈0.01）,且转录表达与其酶活力均呈负相关（P〈0.01）。[结论]砷可能通过调控Cu/Zn-SOD和GSH-Px1的转录表达水平而影响其酶活力,参与砷中毒肝损伤的发生发展。

英文摘要：

[Objective] To analyze the correlation between the transcriptional expressions of Cu/Zn-superoxide dismutase （Cu/Zn-SOD） and glutathione peroxidase （GSH-Px）1 and their enzyme activities in peripheral blood of arsenic-exposed population from a coal-burning area, and to explore their effects on the development of liver injury in endemic arsenism caused by coal-burning. [ Methods ] The arsenic exposure group consisted of 133 people exposed to arsenic （including 25 non-cases and 108 cases） who were selected from the area with endemic arsenism caused by coal-burning. The case group was divided into no obvious hepatopathy group （38 cases） and 2 hepatopathy groups （including 43 mild and 27 moderate-severe cases）. Another 34 normal persons from nonarsenic polluted villages were taken as the control group. Peripheral blood samples were collected from all subjects. The mRNA expressions of Cu/Zn-SOD and GSH-Px1 were detected by real-time quantitative reverse transcription polymerase chain reaction （qPCR）. The activities of SOD, Cu/Zn-SOD and GSH-Px were detected by chemical methods. [ Results ] Compared with the control group, mRNA expressions of Cu/Zn-SOD and GSH-Px 1 in the hepatopathy group were significantly higher （P 〈 0.05 or P 〈 0.01）. Compared with the non-case group, Cu/Zn-SOD mRNA were significantly higher in the hepatopathy group （P〈0.05）. There was no significant difference among case groups. Compared with the control group and the non-case group, activities of SOD, Cu/ZnSOD and GSH-Px decreased obviously in the hepatopathy group （P〈 0.05 or P 〈 0.01）. Compared with the no obvious hepatopathy group, activities of SOD and Cu/Zn-SOD significantly decreased in the mild hepatopathy group （P 〈 0.05）, and activities of SOD, Cu/Zn-SOD and GSH-Px in the moderate-severe hepatopathy group significantly decreased （P〈 0.05 or P〈 0.01）. Compared with the mild hepatopathy group, activities of SOD significantly decreased in the moderate-severe hepatopathy group （P ?