亚砷酸盐
DNA损伤
化学
DNA修复
砷
核苷酸切除修复
DNA
硒
锌指
致癌物
基底切除修复术
生物化学
基因
转录因子
有机化学
作者
A. Hartwig,Holger Blessing,Tanja Schwerdtle,Ingo Walter
出处
期刊:Toxicology
[Elsevier]
日期:2003-10-16
卷期号:193 (1-2): 161-169
被引量:149
标识
DOI:10.1016/j.tox.2003.08.004
摘要
Nickel, cadmium, cobalt and arsenic compounds are well known carcinogens to humans and experimental animals. In addition to the induction of mainly oxidative DNA damage, they interfere with nucleotide and base excision repair (BER) at low, non-cytotoxic concentrations. In case of arsenic, an inactivation of DNA repair has also been observed for the trivalent and pentavalent methylated metabolites, with the strongest effects exerted by MMA(III) and DMA(III). As potential molecular targets, interactions with so-called zinc finger proteins involved in DNA repair and/or DNA damage signaling have been identified. For example, arsenite suppresses poly(ADP-ribosyl)ation at extremely low, environmentally relevant concentrations. Also, Fpg and XPA involved in BER and NER, respectively, are inactivated by arsenite, MMA(III) and DMA(III). Nevertheless, an interaction with the zinc finger structures of DNA repair proteins may also occur by essential trace elements such as certain selenium compounds, which appear to exert anticarcinogenic properties at low concentrations but may compromise genetic stability at higher concentrations.
科研通智能强力驱动
Strongly Powered by AbleSci AI