@inproceedings{oai:jaxa.repo.nii.ac.jp:00013910,
 author = {三浦, ゆり and 加納, まゆみ and 戸田, 年総 and 鈴木, 捷三 and Miura, Yuri and Kano, Mayumi and Toda, Toshifusa and Suzuki, Shozo},
 book = {宇宙利用シンポジウム　第19回　平成14年度, Space Utilization Research: Proceedings of the Nineteenth Space Utilization Symposium},
 month = {Feb},
 note = {To study cell response to low dose oxidative stress, radiation adaptive response (RAR) for cell growth and its molecular mechanism were examined using cultured glial cells. Glial cells cultured from Wistar rats were pre-treated with a low dose of X-rays (0.1 Gy) and subsequently exposed to a challenging dose of X-rays (2 Gy). The decrease of cell growth due to challenging dose of irradiation was suppressed by low dose pre-irradiation. RAR was not observed in the presence of the inhibitors of protein kinase C (PKC) or DNA-dependent protein kinase (DNAPK), and in severe combined immunodeficiency (scid) cells or ataxia-telangiectasia mutated (ATM)-knockout cells. Therefore, PKC, DNAPK, and ATM should be involved in RAR. To study the variant expressions of proteins caused by oxidative stress comprehensively, the effect of H2O2-treatment on the expressions of proteins in glial cells using proteomics was examined. The exposure to H2O2 (100 microM) changed the expression of several spots of proteins in glial cells. Spots of proteins were identified by MALDI-TOF mass spectroscopy after digestion by trypsin in gel. As a result, it was suggested that in glial cells the spot of peroxiredoxin 2 was changed by H2O2-treatment., 資料番号: AA0045438003},
 pages = {6--8},
 publisher = {宇宙科学研究所, The Institute of Space and Astronautical Science (ISAS)},
 title = {グリア細胞の酸化ストレス適応応答機構:細胞学的・プロテオミクス的解析},
 year = {2003}
}