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作 者:安艳[1] 银丽娟[2] 王三祥[3] 王正辉[3] 李贞[1] 商希梅[1] 乔建维[1] 牛静宜[1]
机构地区:[1]山东省医学科学院放射医学研究所,济南250062 [2]贵州省纳雍县疾病预防控制中心 [3]山西省地方病防治研究所
出 处:《卫生研究》2008年第2期237-241,共5页Journal of Hygiene Research
基 金:国家自然科学基金资助项目(No.30540018);教育部留学回国人员科研启动基金(2006);人事部留学回国人员科技活动择优资助项目(2006);山东省优秀中青年科学家科研奖励基金(No.2006BS03067)
摘 要:尿、发、指(趾)甲中砷水平可以反应短期砷接触内剂量,可作为人体内灵敏有效的砷暴露标志物。长期慢性砷接触可以诱发皮肤色素代谢异常和掌跖角化等典型的皮肤病变,尿中MMA(V)可认为是暴露的生物有效剂量。活性氧和抗氧化能力、炎性分子基因表达、外周血淋巴细胞微核和姊妹染色单体互换和染色体畸变是无机砷摄入的早期生物效应标志物。砷易感性标志物包括DNA修复酶、氧化和抗氧化酶、氧化应激相关酶以及异物代谢酶基因组多态性。砷对健康的危害是由于基因组不稳定性和氧化应激等毒理机制而导致的基因-基因、基因-环境交互作用的慢性复杂的渐进性损害。A series of molecular environmental epidemiological studies have been carried out to elucidate biomarkers of exposure, effect, and susceptibility for arsenic-related health hazards in Taiwan Region in China. Arsenic levels in urine, hair, and nail could be biomarkers for short-term internal dose, skin hyperpigmentation and palmoplantar hyperkeratosis could be biomarkers for long-term (many years) internal dose, and percentage of monomethylarsonic acid in total metabolites of inorganic arsenic in urine could be considered as an exposure marker for biologically effective dose. The biomarkers of early biological effects of ingested inorganic arsenic could include blood levels of reactive oxidants and anti- oxidant capacity, genetic expression of inflammatory molecules, as well as cytogenetic changes including sister chromatid exchange, micronuclei, and chromosome aberrations of peripheral lymphocytes. Biomarkers of susceptibility to arsenicinduced health hazards could include genetic polymorphisms of enzymes involved in xenobiotie metabolism, DNA repair, and oxidative stress, as well as serum level of carotenoids. Gene-gene and gene-environment interactions could be involved in arsenic-induced health hazards through toxicological mechanisms including genomic instability and oxidative stress.
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