Enhancement of radiosensitivity by topoisomerase II inhibitor, amrubicin and amrubicinol, in human lung adenocarcinoma A549 cells and kinetics of apoptosis and necrosis induction

• Material Type: 文書・図像類
• Title: Enhancement of radiosensitivity by topoisomerase II inhibitor, amrubicin and amrubicinol, in human lung adenocarcinoma A549 cells and kinetics of apoptosis and necrosis induction
• Author/Editor: HAYASHI, Sachiko; HATASHITA, Masanori; MATSUMOTO, Hideki; SHIOURA, Hiroki; KITAI, Ryuhei; KANO, Eiichi
• Author Heading: HAYASHI, Sachiko; HATASHITA, Masanori; MATSUMOTO, Hideki; SHIOURA, Hiroki; KITAI, Ryuhei; KANO, Eiichi
• Publication, Distribution, etc.: D.A. Spandidos
• Publication Date: 2006-08
• Publication Date (W3CDTF): 2006-08
• Periodical title: International Journal of Molecular Medicine
• No. or year of volume/issue: 18
• Volume: 18
• Pages: 909-915
• ISSN (Periodical Title): ISSN : 1107-3756
• Text Language Code: eng
• Subject Heading: amrubicin; human lung adenocarcinoma A549 cells; enhancement; X-rays; radiosensitivlty; apoptosis; necrosis; topoisomerase Il
• Target Audience: 一般
• Note (General): The effects of amrubicin (AMR) and its active metabolite, amrubicinol (AMROH), on the sensitivity of human lung adenocarcinoma A549 cells to ionizing radiation were investigated in vitro. Further, the kinetics of apoptosis and necrosis induction were also analyzed. The cytocidal efftcts of X-ray irradiation on A549 cells resulted in a low level of radiosensitivity with a D value of 12 Gy. The slopes of the survival curves in the exponential phase were plotted on semilogarithmic paper for radiation combined with AMR (2.5 g/ml) and AMROH (0.02 g/ml) treatment, and were shown to be approximately parallel to treatment with irradiation alone. The initial shoulder-shape portion of the survival curve for radiation alone, indicating the repair of sublethal damage, was reduced as compared to that for sequential combined treatment with AMR or AMROH. Sequential treatments with AMR or AMROH prior to ionizing radiation resulted in an additive radio-enhancement effect that reduced not only survival, but also the shoulder width. Fractionated irradiation with 2 Gy per fraction of A549 cells was carried out in vitro simi1ar to that commonly performed in clinical radiotherapy and the radio-resistance of the cells was shown to be inhibited by AMR and AMROH. Similar to AMR and AMROH, adriamycin and etoposide (VP-16) are DNA topoisomerase II inhibitors. The effects of these 4 agents on cells that received X-ray irradiation were compared and aii of the agents exhibited comparable radio-enhancement effects. The induction of apoptosis was investigated at 48 and 72 h after administraion of AMROH, radiiltion or combined treatment, and apoptosis was not significantly induced after any of the treatments. We also examined the induction of necrosis, and found that the incidence of necrosis following combined treatment was approximately 2 times higher than that with either of the single treatments.
• Source: https://u-fukui.repo.nii.ac.jp/?action=repository_action_common_download&item_id=20100&item_no=1&attribute_id=22&file_no=1
• Access Restrictions: 限定公開
• Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• Original Data Provider (Database): 福井大学 : 福井大学学術機関リポジトリ