Evaluation of DNA damage in patients with arsenic poisoning: urinary 8-hydroxydeoxyguanine.
Evaluation of DNA damage in patients with arsenic poisoning: urinary 8-hydroxydeoxyguanine.
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砷中毒患者DNA损伤评价：尿8-羟基脱氧鸟嘌呤。
DOI：
10.1016/j.taap.2003.10.021
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发表时间：
2004
影响因子：
3.8
通讯作者：
Waalkes,MichaelP
中科院分区：
文献类型：
--
作者：
Yamauchi,Hiroshi;Aminaka,Yoshito;Yoshida,Katsumi;Sun,Guifan;Pi,Jingbo;Waalkes,MichaelP
分析急、慢性砷中毒患者砷暴露与DNA损伤的关系。测量尿 8-羟基脱氧鸟嘌呤 (8-OHdG) 浓度作为 DNA 氧化损伤的指标。在 52 名因意外口服三氧化二砷而发生急性砷中毒的患者中，有 60% 的患者尿液中 8-OHdG 显着升高。这比正常健康受试者 (n = 248) 的水平高出两到三倍。急性中毒后尿液中的砷浓度与 8-OHdG 水平升高之间存在明显的关系。急性砷中毒事件发生后 180 天内，尿 8-OHdG 水平恢复正常。在因饮用砷酸盐 [As(V)] 水平升高的井水而长期中毒的患者中，尿液中 8-OHdG 浓度也升高。在 82 名慢性中毒患者中观察到 8-OHdG 水平与尿液中砷水平之间存在显着相关性。因此，氧化性 DNA 损伤的证据发生在亚砷酸盐 [As(III)] 引起的急性砷中毒和 As(V) 引起的慢性砷中毒中。在提供低砷饮用水的慢性中毒患者中，在高砷摄入量减少后的 9 个月至 1 年内，DNA 损伤的证据消退。最初的砷暴露水平似乎决定了恢复期的长短。这些数据表明，随着停止接触，慢性和急性砷中毒的某些方面可能是可逆的。这些知识可能有助于我们了解砷致癌导致的风险升高，并可能以前瞻性的方式用于评估个人风险。
The relationship between arsenic exposure and DNA damage in patients with acute or chronic arsenic poisoning was analyzed. Urinary 8-hydroxydeoxyguanine (8-OHdG) concentrations were measured as an indication of oxidative DNA damage. A remarkable increase in 8-OHdG in the urine was observed in 60% of 52 patients with acute arsenic poisoning from the accidental oral intake of the arsenic trioxide. This was two- to threefold higher than levels in normal healthy subjects (n = 248). There was a clear relationship between arsenic concentrations in urine after acute poisoning and elevated levels of 8-OHdG. Levels of urinary 8-OHdG returned to normal within 180 days after the acute arsenic poisoning event. In patients chronically poisoned by the consumption of well water with elevated levels of arsenate [As(V)], elevated 8-OHdG concentrations in urine were also observed. A significant correlation between the 8-OHdG levels and arsenic levels in the urine was observed in 82 patients with chronic poisoning. Thus, evidence of oxidative DNA damage occurred in acute arsenic poisoning by arsenite [As(III)] and in chronic arsenic poisoning by As(V). In chronic poisoning patients provided low-arsenic drinking water, evidence of DNA damage subsided between 9 months and 1 year after the high levels of arsenic intake were reduced. The initial level of arsenic exposure appeared to dictate the length of this recovery period. These data indicate that some aspects of chronic and acute arsenic poisoning may be reversible with the cessation of exposure. This knowledge may contribute to our understanding of the risk elevation from arsenic carcinogenesis and perhaps be used in a prospective fashion to assess individual risk.