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  4. Mechanism of cytotoxicity and resistance of ar senic tr ioxide in cancer cells
 
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Mechanism of cytotoxicity and resistance of ar senic tr ioxide in cancer cells

Date Issued
1999-07-31
Date
1999-07-31
Author(s)
陳耀昌
DOI
882314B002064
URI
http://ntur.lib.ntu.edu.tw//handle/246246/27317
Abstract
Arsenic trioxide is a novel anticancer agent, which has been found to induce remission in acute promyelocytic leukemic patients following daily intravenous administration. The therapeutic value of arsenic trioxide in other cancers is still largely unknown. Our previous study showed that bladder cancer, acute promyelocytic leukemic and gastrointestinal cancer cells were the most sensitive to arsenic trioxide. Cellular glutathione system plays an important role in arsenic detoxification in mammalian cells. Cancer cells that were intrinsically sensitive to arsenic trioxide contained lower levels of glutathione whereas resistant cancer cells contained higher levels of glutathione. On the other hand, there was no association of glutathione-s-transferase-pi or multidrug resistance-associated protein 1 levels with arsenic sensitivity in these cancer cells. In the present study we have shown that multidrug resistant cancer cells that were cross-resistant to arsenic contained higher levels of glutathione or multidrug-resistance associated protein 1 than their drug-sensitive parental cells. Cancer cells become more sensitive to arsenic after depletion of cellular glutathione with L-buthionine sulfoximine. We concluded that cellular glutathione level is the most important determinant of arsenic sensitivity in cancer cells. Cellular glutathione level and its modulation by buthionine sulfoximine should be considered in designing clinical trials using arsenic in solid tumors.
Subjects
氧化砷
癌症治療
抗藥性
SDGs

[SDGs]SDG3

Publisher
臺北市:國立臺灣大學醫學院檢驗醫學科
Type
journal article
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882314B002064.pdf

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