Mechanism of enhancement of heat-induced apoptosis by Tempo in PC12 cells

• ZHAO Qing-Li

  Dept. Radiol. Sci., Toyama Med. and Pharmaceut. Univ.

• FUJIWARA Yoshisada

  Dept. Radiol. Sci., Toyama Med. and Pharmaceut. Univ.

• KONDO Takashi

  Dept. Radiol. Sci., Toyama Med. and Pharmaceut. Univ.

抄録

Tempo, a nitroxide, exerts an SOD-like antioxidant activity against ROS. Reportedly, Tempo inhibits ROS-induced apoptosis in thymocytes, and activates JNK1 to induce apoptosis in breast cancer cells. In this present study, we observed sensitization of heat-induced apoptosis by 5 mM Tempo in the pheochromocytoma cell line (PC12). We investigated the sensitization mechanisms. 5 mM Tempo or 44C/10 min heating was non-apoptotic to PC12 cells. However, the combined treatment markedly sensitized PC12 cells to apoptosis, as induced by 44C/30 min. Although levels of Bcl-2, Bcl-XL and Bax in lysates were not altered, Bax was rapidly translocated to mitochondria after the combined treatment and 44C/30 min, followed by cytochrome c release. The combined treatment and 44C/30 min activated JNK 1, which was partially inhibited by the inhibitors of JNK. Our results suggest that sensitization of Tempo/heat-induced apoptosis may involve Bax-mediated increase in outer mitochondrial membrane permeability resulting in cytochrome c release.

収録刊行物

• 日本放射線影響学会大会講演要旨集

  日本放射線影響学会大会講演要旨集 2005 (0), 330-330, 2005

  一般社団法人 日本放射線影響学会

詳細情報

• CRID: 1390282680618115200
• NII論文ID: 130007000868
• DOI: 10.11513/jrrsabst.2005.0.330.0
• 本文言語コード: en
• 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