@article{oai:tohoku-mpu.repo.nii.ac.jp:00000023,
 author = {髙橋, 昌悟 and Takahashi, Shogo and 三浦, 彩佳 and Miura, Ayaka and 佐々木, 瞳 and Sasaki, Hitomi and 坂口, 修平 and Sakaguchi, Shuhei and 永田, 清 and Nagata, Kiyoshi},
 issue = {59},
 journal = {東北薬科大学研究誌, Journal of Tohoku Pharmaceutical University},
 month = {Dec},
 note = {We examained the contribution of iron to the cytotoxicity of tumor necrosis factor (TNF)-a combined with actinomycin D (ActD) as a model of hepatocyte injury in Hep G2 cells. In general,hepatocytes are resistant to TNF-a. However,a transcriptional inhibitor such as ActD can sensitize then to TNF-a. In the present study, we show that low levels of ActD (0.5nM) sensitized HepG2 cells to the cytotoxic effects of TNF-a (20 ng/mL) for 48h. Iron plays a critical role in catalyxing the formation of potent oxidants. To acsses the toxicological significance of this TNF-a/ActD interaction,ferric-nitrilotriacetate (Fe-NTA,2uM) was added to the cells. Treatment with Fe-NTA significantly increased the sensitivity to the TNF-a/ActD-mediated cell death. TNF-a/ActD-mediated cell death in the presence of a lower concentration of iron did not result in DNA fragmentation. We suggest that iron increased the sensitivity to the cytotoxicity of TNF-a/ActD in HepG2 cells. It is likely that TNF-a/ActD/Fe-NTA-mediated cell death contributes to the non-apoptotic death of cells via oxidative stress caused by iron. Our experimental model may be useful for studying hepatic drug metabolism using TNF-a as a hepatocyte injury,especially in HepG2 cells.},
 pages = {69--74},
 title = {鉄存在下HepG2細胞におけるTNF-α/actinomycin D処理による肝障害モデルの構築},
 year = {2012},
 yomi = {タカハシ, ショウゴ and ミウラ, アヤカ and ササキ, ヒトミ and サカグチ, シュウヘイ and ナガタ, キヨシ}
}