過酸化水素の細胞毒性に対するコバルトの効果

  • 藤原 宏之
    山形大学・工学部・応用生命システム工学科
  • 渕上 弥史
    山形大学・工学部・応用生命システム工学科
  • 野村 保友
    山型大学大学院・医学系研究科・生命環境医科学専攻
  • 馮 忠剛
    山形大学・工学部・応用生命システム工学科
  • 中村 孝夫
    山型大学大学院・医学系研究科・生命環境医科学専攻

書誌事項

タイトル別名
  • Alteration in oxidative stress responses by the pretreatment with cobalt

説明

Cytotoxicity by reactive oxygen species (ROS) are mainly resulted from the reaction with biological molecules. Recently, it was reported that mitochondrial DNA (mtDNA) damage was induced by CoCl2 through ROS. However, there are only a few reports indicating cytotoxicity of CoCl2 at the same concentration. Here, we evaluated cell growth, DNA damage and expression of hypoxia inducible factor-1α relevant to the treatment with CoCl2 in order to determine the responses of 293 cells in detail. For the estimation of DNA damage, we used long PCR method for mtDNA and nuclear-encoded β-globin gene (nDNA). When cells were incubated with 0.4 mM H2O2 for 1 hr, mtDNA damage occurred but nDNA remained unchanged. The cell growth was suppressed completely 2 days after the treatment and cell number decreased within 4 days. In the case of CoCl2 treatment at 100 μM for 24 hr, cell number was the same as that without any treatment throughout the experiment, suggesting that CoCl2 did not cause cytotoxicity. Furthermore, western blots revealed the activation of hypoxia inducible factor-1α under the conditions. When cells was exposed to 100 μM CoCl2 for 24 hr prior to 0.4 mM H2O2 treatment for 1 hr, we observed a transient growth arrest and the cell number increased after 4days of the treatment of H2O2. These data indicate that the pretreatment of CoCl2 cause the suppression of cytotoxicity by H2O2 rather than the induction. [Jpn J Physiol 55 Suppl:S77 (2005)]

収録刊行物

詳細情報 詳細情報について

  • CRID
    1390001205728206592
  • NII論文ID
    130005448032
  • DOI
    10.14849/psjproc.2005.0_s77_3
  • データソース種別
    • JaLC
    • CiNii Articles
  • 抄録ライセンスフラグ
    使用不可

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