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Accession number;02A0304392
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| Title;Anticancer mechanism of free radical induced by cationic Fe-porphyrin. |
| Author;
KAWAKAMI HIROYOSHI
(Grad. Sch. of Tokyo Metrop. Univ.)
KASUGAI NOBUYOSHI
(Grad. Sch. of Tokyo Metrop. Univ.)
ASAYAMA SHOICHIRO
(Grad. Sch. of Tokyo Metrop. Univ.)
NAGAOKA SHOJI
(Grad. Sch. of Tokyo Metrop. Univ.)
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Journal Title;Abstracts. Symposium on Biofunctional Chemistry
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Journal Code:L0836A
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ISSN:
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VOL.16th;NO.;PAGE.72-73(2001)
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| Figure&Table&Reference; |
| Pub. Country;Japan |
| Language;Japanese |
| Abstract;A number of cancer cells are known to generate a large amount of O2- and release it from themselves because of their low SOD activity. Fe-porphyirn derivatives as SOD mimic convert intracellular O2- to H2O2 and can directly interact with H2O2 to generate OH. We have reported that a water-soluble cationic Fe-porphyrin (FeMPy2P2P) with SOD activity show the selective cytotoxicity between cancer cells and normal cell. We believe that the cyiotoxicity of FeMPy2P2P simply depends on not only SOD activity but also catalase activity of cells. In this study, we measured the SOD activity and catalase activity of human cells. It is well known that N-acetylcystene(NAC) is a glutathione (GSH) precursor and increases the intracellular GSH levels so that NAC inhibits the intracellular H2O2 generation. We have demonstrated that NAC inhibits cell death induced by FeMPy2P2P. This result indicates that the intracellular H2O2 generated by FeMPy2P2P is responsible for the induction of cell death. Additionally, we will discuss the anticancer mechanism of FeMPy2P2P using transformed cell lacking SOD. (author abst.) |
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