کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2570987 | 1128611 | 2008 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Low concentration of arsenite exacerbates UVR-induced DNA strand breaks by inhibiting PARP-1 activity
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کلمات کلیدی
SSBDSBPBSPARP-1UVRBER8-OHdGBSA - BSANER - DOWNSmall interfering RNA - RNA تداخل کوچکROS - ROSsiRNA - siRNASodium arsenite - آرسنیت سدیمArsenic - آرسنیکbovine serum albumin - آلبومین سرم گاوUltraviolet radiation - اشعه ماوراء بنفشnucleotide excision repair - تعمیر مجدد نوکلئوتیدیbase excision repair - تعمیر پایه پایهComet assay - روش کامت یا روش سنجش ستاره دنبالهدار Carcinogenesis - سرطانزاییdouble-strand break - شکست دو ردیفsingle-strand break - شکستن تک رشتهDNA strand break - شکستن رشته DNAPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریDHE - وPoly(ADP-ribose) polymerase-1 - پلی (ADP-ribose) پلیمراز-1Reactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
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چکیده انگلیسی
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 (â¤Â 2 µM) alone did not induce significant DNA strand breaks, but greatly enhanced the DNA strand breaks induced by UVR. Further studies showed that 2 µM 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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology and Applied Pharmacology - Volume 232, Issue 1, 1 October 2008, Pages 41-50
Journal: Toxicology and Applied Pharmacology - Volume 232, Issue 1, 1 October 2008, Pages 41-50
نویسندگان
Xu-Jun Qin, Laurie G. Hudson, Wenlan Liu, Graham S. Timmins, Ke Jian Liu,