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Arsenic Toxicity induces ROS activity and DNA damage leads to G0/G1 arrest in Fibroblast maybe one of Carcinogensis Mechanism

http://hdl.handle.net/10458/6274
http://hdl.handle.net/10458/6274
2d1a6d16-6a11-4a10-ba05-b111a8ce0845
Item type その他 / Others(1)
公開日 2020-06-21
タイトル
タイトル Arsenic Toxicity induces ROS activity and DNA damage leads to G0/G1 arrest in Fibroblast maybe one of Carcinogensis Mechanism
言語 en
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_1843
資源タイプ other
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Jutapon, Chayapon

× Jutapon, Chayapon

WEKO 29959

en Jutapon, Chayapon

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Harishkumar, Madhyastha

× Harishkumar, Madhyastha

WEKO 29960

en Harishkumar, Madhyastha

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Nakajima, Yuichi

× Nakajima, Yuichi

WEKO 29961

en Nakajima, Yuichi

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丸山, 眞杉

× 丸山, 眞杉

WEKO 2630

en Maruyama, Masugi

ja 丸山, 眞杉

ja-Kana マルヤマ, マスギ


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内容記述タイプ Abstract
内容記述 Many of toxico-epidemiologic studies demonstrated that arsenic is pollutant. It associates with worldwide human health problems. Arsenic is assumed as tumor activity inducer. The exactly mechanism of arsenic induced genotoxicity or carcinogenesis are still in doubt. To investigate the mechanism of alsenic-induced carcinogenesis and alteration of cell cycle, we exposed mouse fibroblast cells with various concentrations of arsenIcals. Firstly, we checked how arsenic acts on fibroblast cells viability. MTTa ssays shown, high degree of cell viability was observed in the lower arsenic concentration (≤50μM). Meanwhile, the higher concentration (above of 50μM), reduction of cells viability can be seen. AlsenIc toxicity on fibroblast cells was examined by LDH assays. Increasing of arsenic concentration, LDH activity was also increased. Thus, arsenic toxicity effect was said to be dose-dependent. Therefore, we investigated whether arsenic contributed on generation of intracellular reactive oxygen species (ROS) or not. ROS assays and ROS fluorescence image showed the activity in a manner of dose dependent, in lower concentrations (<500μM). 8-OHdG immunohistochemistry indicated that arsenic exposure induced oxidative stress and DNA damage. We examined effect of arsenic on the apoptosis and cell death by TUNEL assays. Interestingly, there had no apoptosis evidence in the lower dosage of arsenic (≤100μM). Furthermore,we observed DNA damage check-point and alteration of cell cycle. Flow cytometer analysis and western blotting result revealed that arsenic conducted cell cycle arrest in G0/G1 phase. This alteration was regulated through ATM/ATR pathway by enhancing the expression of pATM, pATR, p53, and Chk-2. Our study shown that, in an adequate dosage, arsenic prevents fibroblast cells death and arrests cell cycle in G0/G1 phase,through phosphatidylinositol-3-kinase (PI3K)-related kinases. Our first step of studying can be assumed that, arsenic is possible to induce carcinogenesis by convincing DNA damage, prolonging cell cycle and extending cell survival.
言語 en
書誌情報 en : 4th InternationalArsenic Symposium in MIYAZAKI 2015

p. 66-66, 発行日 2015-10
出版者
出版者 University of Miyazaki, IRISH
言語 en
著者版フラグ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
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