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

Keywords

  • Apoptosis
  • Necrosis
  • Nitric oxide
  • Peroxynitrite

ASJC Scopus subject areas

  • Health, Toxicology and Mutagenesis
  • Pharmacology
  • Toxicology

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