首页> 外文期刊>Mutation Research, A. Reviews in Genetic Toxicology >Genetic, cytogenetic, and carcinogenic effects of radon: a review
【24h】

Genetic, cytogenetic, and carcinogenic effects of radon: a review

机译:don的遗传,细胞遗传和致癌作用:综述

获取原文
获取原文并翻译 | 示例
       

摘要

Radon exposure has been linked to lung carcinogenesis in both human and animal studies. Studies of smoking and nonsmoking uranium miners indicate that radon alone is a risk factor for lung cancer at the levels encountered by these miners, although thepossibility exists that other substances in the mine environment affect the radon-induced response. The relevance of data from mines to the lower-exposure home environment is often questioned; still, a recent study of miners exposed to relatively low radon concentrations demonstrated a statistically significant increase for lung and laryngeal cancer deaths. In two major series of experiments with rats, the primary carcinogenic effect found was respiratory tract tumors, and evidence for an inverse exposure-rate effect was also noted. Although this inverse dose-rate effect also has been described in underground miner studies, it may not similarly apply to radou in the home environment. This observation is due to the fact that, below a certain exposure,cells are hit once or not at all, and one would not expect any dose-rate effect, either normal or inverse. Because some chromosome aberrations persist in cycling cells as stable events, cytogenetic studies with radon are being performed to help completethe understanding of the events leading to radon-induced neoptasia. Radon has been found to indued 13 times as much cytogenetic damage (as measttred by the occurrence of micronuclei) than a similar dose of Co. A wide variety of mutation systems have demonstrated alpha-particle mutagenesis; recent investigations have focused on the molecular basis of alpha-induced mutagenesis, Gene mutations are induced by radon in a linear and dose-dependent fashion, and with a high biological effect relative to low-LETirradiation. Studies of the hprt locus show that approximately half of the alpha-induced mutations arise by complete deletion of the gene the remaining mutations are split between partial deletions, rearrangements) and events not detectable by Southernblot or PCR exon analysis. Although other mutation systems do not show the sum spectra, as observed in the hprt gene (suggesting that the gene environment affects response), DMA deletions or multilocus lesions of various size appear to be predominant, after radon exposure. As data emerge regarding radon-induced changes at the chromosomal and molecular level, the mechanisms involved in radon carcinogenesis are being clarified. This information should increase the understanding of risk at the low exposurelevels typically found in the home.
机译:在人类和动物研究中,exposure的暴露均与肺癌发生有关。吸烟和不吸烟的铀矿工的研究表明,尽管矿井环境中的其他物质可能影响the诱发的反应,但在这些矿工遇到的水平上,单独的ra是肺癌的危险因素。人们经常质疑从地雷到低暴露家庭环境的数据的相关性;尽管如此,最近对of气浓度相对较低的矿工的一项研究表明,肺癌和喉癌的死亡率有统计学上的显着增加。在大鼠的两个主要实验系列中,发现的主要致癌作用是呼吸道肿瘤,并且还指出了暴露速率反作用的证据。尽管这种反向剂量率效应在地下矿工研究中也已有描述,但可能不适用于家庭环境中的radou。该观察结果是由于以下事实:在一定暴露量以下,细胞被击中一次或根本没有被击中,并且人们不会期望任何剂量率效应,无论是正常的还是相反的。由于某些染色体畸变会作为稳定事件在循环细胞中持续存在,因此正在进行ra的细胞遗传学研究,以帮助完成对导致ra诱发的神经病的事件的理解。已发现比类似剂量的Co具有13倍的细胞遗传学损伤(受微核的发生所抑制)。多种突变系统已证明具有α粒子诱变作用。最近的研究集中在α诱导的诱变的分子基础上,Gene以线性和剂量依赖的方式诱导基因突变,并且相对于低LET辐照具有高生物学效应。 hprt基因座的研究表明,大约有一半的α诱导的突变是由于基因的完全缺失而产生的,其余突变分为部分缺失,重排和无法通过Southernblot或PCR外显子分析检测到的事件。尽管其他突变系统未显示总谱,如在hprt基因中观察到的(暗示基因环境会影响响应),但,暴露后DMA缺失或各种大小的多位点病变似乎是主要的。随着有关ra引起的染色体和分子水平变化的数据的出现,ra致癌作用的机制正在阐明。此信息应增加对房屋中通常存在的低暴露水平风险的理解。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号