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Hyperoxia activates ATM independent from mitochondrial ROS and dysfunction
High levels of oxygen (hyperoxia) are often used to treat individuals with respiratory distress, yet prolonged hyperoxia causes mitochondrial dysfunction and excessive reactive oxygen species (ROS) that can damage molecules such as DNA. Ataxia telangiectasia mutated (ATM) kinase is activated by nucl...
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| 出版年: | Redox Biol |
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| 主要な著者: | , , , |
| フォーマット: | Artigo |
| 言語: | Inglês |
| 出版事項: |
Elsevier
2015
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| 主題: | |
| オンライン･アクセス: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4430709/ https://ncbi.nlm.nih.gov/pubmed/25967673 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.redox.2015.04.012 |
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