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作 者:陈敏[1] 朴丰源[1] 孙鲜策[1] 李秋娟[1] 杨光[1] 叶建新[1] 曲淑贤[1] 刘晓芳[1]
出 处:《中国公共卫生》2008年第3期373-374,共2页Chinese Journal of Public Health
基 金:国家自然科学基金(30571584;30600488);辽宁省教育厅基金项目(05L113)
摘 要:目的通过检测活性氮族引起的核酸损伤标志物8-硝基鸟嘌呤(8-NO2-G)在砷暴露小鼠心肌组织中的表达情况,探讨砷对心肌细胞的毒性作用机制。方法昆明种小鼠40只,随机分为4组:1,2,4mg/L三氧化二砷染毒组和生理盐水组。连续染毒60d,取小鼠心脏组织固定,用免疫组化方法观察心肌细胞的8-NO2-G表达。结果对照组小鼠心肌细胞中无8-NO2-G表达,而砷暴露组小鼠心肌细胞的胞浆被染成棕褐色,呈现抗8-NO2-G阳性反应,4mg/L剂量染砷组小鼠心肌细胞中8-NO2-G表达明显。结论慢性砷暴露可诱发小鼠心肌细胞8-NO2-G的高表达,提示8-NO2-G可能是砷致心肌细胞损伤的早期生物标志物。Objective To explore the molecular mechanism of arsenic toxicology to cardiac muscle cell by detecting the expression of 8-nitroguanine,which was the biochemical marker of nuclear acid damage induced by reactive nitrogen species(RNS).Methods Different concentrations of trioxide arsenic(As2O3)were administered to mice for consecutive 60 days,followed by decollation.Pathologic changes of cardiac muscle cell were detected by HE coloration.Immunohistochemistry method was used to investigate 8-nitroguanine(8-NO2-G)expression in cardiac muscle cell of mice.Results Pathologic changes were observed in 1,2 and 4ppm groups.The expression of 8-NO2-G increased significantly in experimental groups and was in a dose-effect relation(P〈0.05).Conclusion The low dose exposure of mice to arsenic RNS may result in high expression of 8-NO2-G.It indicated that the 8-NO2-G may be the early bio-marker of cardiac muscle cell damage induced by arsenic.
关 键 词:三氧化二砷 心肌 8-硝基鸟嘌呤 免疫组化 核酸损伤
分 类 号:R114[医药卫生—卫生毒理学]
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