| pubmed-article:18619636 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18619636 | lifeskim:mentions | umls-concept:C0086045 | lld:lifeskim |
| pubmed-article:18619636 | lifeskim:mentions | umls-concept:C0872150 | lld:lifeskim |
| pubmed-article:18619636 | lifeskim:mentions | umls-concept:C0032405 | lld:lifeskim |
| pubmed-article:18619636 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:18619636 | lifeskim:mentions | umls-concept:C1428200 | lld:lifeskim |
| pubmed-article:18619636 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:18619636 | lifeskim:mentions | umls-concept:C0205251 | lld:lifeskim |
| pubmed-article:18619636 | lifeskim:mentions | umls-concept:C0052418 | lld:lifeskim |
| pubmed-article:18619636 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:18619636 | pubmed:dateCreated | 2008-9-22 | lld:pubmed |
| pubmed-article:18619636 | pubmed:abstractText | Epidemiological studies have associated arsenic exposure with many types of human cancers. Arsenic has also been shown to act as a co-carcinogen even at low concentrations. However, the precise mechanism of its co-carcinogenic action is unknown. Recent studies indicate that arsenic can interfere with DNA-repair processes. Poly(ADP-ribose) polymerase (PARP)-1 is a zinc-finger DNA-repair protein, which can promptly sense DNA strand breaks and initiate DNA-repair pathways. In the present study, we tested the hypothesis that low concentrations of arsenic could inhibit PAPR-1 activity and so exacerbate levels of ultraviolet radiation (UVR)-induced DNA strand breaks. HaCat cells were treated with arsenite and/or UVR, and then DNA strand breaks were assessed by comet assay. Low concentrations of arsenite (<or=2 microM) alone did not induce significant DNA strand breaks, but greatly enhanced the DNA strand breaks induced by UVR. Further studies showed that 2 microM arsenite effectively inhibited PARP-1 activity. Zinc supplementation of arsenite-treated cells restored PARP-1 activity and significantly diminished the exacerbating effect of arsenite on UVR-induced DNA strand breaks. Importantly, neither arsenite treatment, nor zinc supplementation changed UVR-triggered reactive oxygen species (ROS) formation, suggesting that their effects upon UVR-induced DNA strand breaks are not through a direct free radical mechanism. Combination treatments of arsenite with PARP-1 inhibitor 3-aminobenzamide or PARP-1 siRNA demonstrate that PARP-1 is the target of arsenite. Together, these findings show that arsenite at low concentration exacerbates UVR-induced DNA strand breaks by inhibiting PARP-1 activity, which may represent an important mechanism underlying the co-carcinogenicity of arsenic. | lld:pubmed |
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| pubmed-article:18619636 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18619636 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18619636 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18619636 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:18619636 | pubmed:issn | 1096-0333 | lld:pubmed |
| pubmed-article:18619636 | pubmed:author | pubmed-author:LiuKe JianKJ | lld:pubmed |
| pubmed-article:18619636 | pubmed:author | pubmed-author:TimminsGraham... | lld:pubmed |
| pubmed-article:18619636 | pubmed:author | pubmed-author:WenlanLiuL | lld:pubmed |
| pubmed-article:18619636 | pubmed:author | pubmed-author:HudsonLaurie... | lld:pubmed |
| pubmed-article:18619636 | pubmed:author | pubmed-author:QinXu-JunXJ | lld:pubmed |
| pubmed-article:18619636 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18619636 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:18619636 | pubmed:volume | 232 | lld:pubmed |
| pubmed-article:18619636 | pubmed:owner | NLM | lld:pubmed |
