S-nitrosoglutathione and hypoxia-inducible factor-1 confer chemoresistance against carbamoylating cytotoxicity of BCNU in rat C6 glioma cells

Ding I. Yang, Shang Der Chen, Jiu Haw Yin, Chung Y. Hsu

研究成果: 雜誌貢獻文章

7 引文 (Scopus)

摘要

BCNU (1,3-bis[2-chloroethyl]-1-nitrosourea) is the mainstay in glioblastoma multiform chemotherapy with only minimal effects. BCNU may kill tumor cells via carbamoylating cytotoxicity, which irreversibly inhibits glutathione reductase with resultant accumulation of oxidized form of glutathione causing oxidative stress. S-nitrosoglutathione (GSNO) is a product of glutathione and nitric oxide interaction. We report that GSNO formation may underlie carbamoylating Chemoresistance mediated by activation of inducible nitric oxide synthase. Transactivation of hypoxia-inducible factor-1 (HIF-1)-responsive genes reduces oxidative stress caused by glutathione depletion. We also noted that preconditioning of C6 glioma cells to induce HIF-1 and its downstream genes confers Chemoresistance against carbamoylating cytotoxicity of BCNU.
原文英語
頁(從 - 到)229-234
頁數6
期刊Annals of the New York Academy of Sciences
1042
DOIs
出版狀態已發佈 - 2005

指紋

S-Nitrosoglutathione
Hypoxia-Inducible Factor 1
Carmustine
Cytotoxicity
Glioma
Rats
Glutathione
Oxidative stress
Oxidative Stress
Genes
Chemotherapy
Glutathione Disulfide
Glutathione Reductase
Nitric Oxide Synthase Type II
Glioblastoma
Transcriptional Activation
Tumors
Nitric Oxide
Chemical activation
Cells

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

引用此文

S-nitrosoglutathione and hypoxia-inducible factor-1 confer chemoresistance against carbamoylating cytotoxicity of BCNU in rat C6 glioma cells. / Yang, Ding I.; Chen, Shang Der; Yin, Jiu Haw; Hsu, Chung Y.

於: Annals of the New York Academy of Sciences, 卷 1042, 2005, p. 229-234.

研究成果: 雜誌貢獻文章

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abstract = "BCNU (1,3-bis[2-chloroethyl]-1-nitrosourea) is the mainstay in glioblastoma multiform chemotherapy with only minimal effects. BCNU may kill tumor cells via carbamoylating cytotoxicity, which irreversibly inhibits glutathione reductase with resultant accumulation of oxidized form of glutathione causing oxidative stress. S-nitrosoglutathione (GSNO) is a product of glutathione and nitric oxide interaction. We report that GSNO formation may underlie carbamoylating Chemoresistance mediated by activation of inducible nitric oxide synthase. Transactivation of hypoxia-inducible factor-1 (HIF-1)-responsive genes reduces oxidative stress caused by glutathione depletion. We also noted that preconditioning of C6 glioma cells to induce HIF-1 and its downstream genes confers Chemoresistance against carbamoylating cytotoxicity of BCNU.",
keywords = "Alkylation, Carbamoylation, Chemoresistance, Chemotherapy, Hypoxia, iNOS, Nitric oxide",
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AU - Yang, Ding I.

AU - Chen, Shang Der

AU - Yin, Jiu Haw

AU - Hsu, Chung Y.

PY - 2005

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AB - BCNU (1,3-bis[2-chloroethyl]-1-nitrosourea) is the mainstay in glioblastoma multiform chemotherapy with only minimal effects. BCNU may kill tumor cells via carbamoylating cytotoxicity, which irreversibly inhibits glutathione reductase with resultant accumulation of oxidized form of glutathione causing oxidative stress. S-nitrosoglutathione (GSNO) is a product of glutathione and nitric oxide interaction. We report that GSNO formation may underlie carbamoylating Chemoresistance mediated by activation of inducible nitric oxide synthase. Transactivation of hypoxia-inducible factor-1 (HIF-1)-responsive genes reduces oxidative stress caused by glutathione depletion. We also noted that preconditioning of C6 glioma cells to induce HIF-1 and its downstream genes confers Chemoresistance against carbamoylating cytotoxicity of BCNU.

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KW - Chemotherapy

KW - Hypoxia

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KW - Nitric oxide

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