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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/10458/62742d1a6d16-6a11-4a10-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× Harishkumar, Madhyastha× Nakajima, Yuichi× 丸山, 眞杉 |
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| 抄録 | ||||||
| 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 |
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| 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 | |||||
