DNA Damage Signaling in Human Skin Cells Exposed to Hexavalent Chromium

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11150%2F09%3A00208684" target="_blank" >RIV/00216208:11150/09:00208684 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00179906:_____/09:00201687

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

DNA Damage Signaling in Human Skin Cells Exposed to Hexavalent Chromium

Popis výsledku v původním jazyce

The purpose of this study was to investigate the initial stages of Cr (VI)-induced DNA damaging in normal human skin fibroblasts. Primary human skin fibroblasts were exposed to Cr (VI) at a concentration range of 1-50 ?M during 24 h. Our results confirmthat Cr (VI) dose-dependently stimulates both directly (via its reactive metabolic intermediates) and indirectly (through generated oxidative stress) DNA damaging which results in the activation of DNA damage response pathway during 24 h of treatment. The important members of this pathway include ATM/ATR kinases which stimulate their downstream targets Chk1, Chk2 and p53 in mediating transient G2/M cell cycle arrest and activating cell death characterized by the specific cleavage of PARP. Inhibition ofATM/ATR pathway and suppresion of oxidative stress in exposed cells significantly suppressed cell damage characterized by specific PARP cleavage.

Název v anglickém jazyce

DNA Damage Signaling in Human Skin Cells Exposed to Hexavalent Chromium

Popis výsledku anglicky

The purpose of this study was to investigate the initial stages of Cr (VI)-induced DNA damaging in normal human skin fibroblasts. Primary human skin fibroblasts were exposed to Cr (VI) at a concentration range of 1-50 ?M during 24 h. Our results confirmthat Cr (VI) dose-dependently stimulates both directly (via its reactive metabolic intermediates) and indirectly (through generated oxidative stress) DNA damaging which results in the activation of DNA damage response pathway during 24 h of treatment. The important members of this pathway include ATM/ATR kinases which stimulate their downstream targets Chk1, Chk2 and p53 in mediating transient G2/M cell cycle arrest and activating cell death characterized by the specific cleavage of PARP. Inhibition ofATM/ATR pathway and suppresion of oxidative stress in exposed cells significantly suppressed cell damage characterized by specific PARP cleavage.

Druh

C - Kapitola v odborné knize

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

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Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2009

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název knihy nebo sborníku

New Research on DNA Damage

ISBN

978-1-60456-581-2

Počet stran výsledku

18

Strana od-do

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Počet stran knihy

410

Název nakladatele

Nova Sciense Publishers

Místo vydání

New York

Kód UT WoS kapitoly

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