Mechanisms of cell death induced by nitric oxide and peroxynitrite in Calu-1 cells

Ying J. Wang, Yuan Soon Ho, Min Hsiung Pan, Jen K. Lin

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

S-nitrosoglutathione (GSNO) is an important physiological redox form of nitric oxide (NO) and serves as an NO-releasing compound. 3-Morpholinosydnonimine hydrochloride (SIN-1) produces NO and superoxide anion (O2.-) which results in the formation of peroxynitrite (ONOO-). We investigate the cytotoxicity, cell death mechanisms and gene expression of NO and ONOO- in human lung epithelial cells show NO induced apoptosis and DNA genomic fragmentation. Whereas, ONOO- induced cell death more characteristic of necrosis than apoptosis. The concentrations of GSNO and SIN-1 required to cause death in 50% of cells were greater than 1 mM. Several gene products are important in controling the apoptotic and necrotic processes. Of these, bcl-2, bax and hsp 70 were studied. The level of expression of bcl-2 was dramatically decreased in cells treated with SIN-1 or GSNO, while the expression level of bar, the heterodimer of bcl-2, did not significant change. In addition, a roughly two-fold increase of hsp 70 was found in cells treated with SIN-1. There were no significant changes in hsp 70 levels in cells treated with GSNO.

Original languageEnglish
Pages (from-to)35-44
Number of pages10
JournalEnvironmental Toxicology and Pharmacology
Volume6
Issue number1
DOIs
Publication statusPublished - Aug 4 1998

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Peroxynitrous Acid
Cell death
Nitric Oxide
Cell Death
S-Nitrosoglutathione
Apoptosis
DNA Fragmentation
Cytotoxicity
Gene expression
Superoxides
Oxidation-Reduction
Cause of Death
Necrosis
Genes
Epithelial Cells
Gene Expression
Lung
DNA

Keywords

  • Apoptosis
  • Necrosis
  • Nitric oxide
  • Peroxynitrite

ASJC Scopus subject areas

  • Health, Toxicology and Mutagenesis
  • Pharmacology
  • Toxicology

Cite this

Mechanisms of cell death induced by nitric oxide and peroxynitrite in Calu-1 cells. / Wang, Ying J.; Ho, Yuan Soon; Pan, Min Hsiung; Lin, Jen K.

In: Environmental Toxicology and Pharmacology, Vol. 6, No. 1, 04.08.1998, p. 35-44.

Research output: Contribution to journalArticle

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AB - S-nitrosoglutathione (GSNO) is an important physiological redox form of nitric oxide (NO) and serves as an NO-releasing compound. 3-Morpholinosydnonimine hydrochloride (SIN-1) produces NO and superoxide anion (O2.-) which results in the formation of peroxynitrite (ONOO-). We investigate the cytotoxicity, cell death mechanisms and gene expression of NO and ONOO- in human lung epithelial cells show NO induced apoptosis and DNA genomic fragmentation. Whereas, ONOO- induced cell death more characteristic of necrosis than apoptosis. The concentrations of GSNO and SIN-1 required to cause death in 50% of cells were greater than 1 mM. Several gene products are important in controling the apoptotic and necrotic processes. Of these, bcl-2, bax and hsp 70 were studied. The level of expression of bcl-2 was dramatically decreased in cells treated with SIN-1 or GSNO, while the expression level of bar, the heterodimer of bcl-2, did not significant change. In addition, a roughly two-fold increase of hsp 70 was found in cells treated with SIN-1. There were no significant changes in hsp 70 levels in cells treated with GSNO.

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