Activation of nitric oxide synthase is involved in tamoxifen-induced apoptosis of human erythroleukemia K562 cells

Mauro Maccarrone, Cristina Fantini, Marco Ranalli, Gerry Melino, Alessandro Finazzi Agrò

Research output: Contribution to journalArticlepeer-review

Abstract

Tamoxifen induces apoptosis (programmed cell death) in human erythroleukemia K562 cells. Nitric oxide synthase activity and expression increased in apoptotic cells by 315% and 280%, respectively, compared to controls. The specific inhibitor of nitric oxide synthase, l-NAME, protected K562 cells from tamoxifen-induced apoptosis, whereas the nitric oxide donor, sodium nitroprusside (SNP), potentiated the apoptotic effect of the drug. In addition, 5-lipoxygenase was activated by tamoxifen and the specific enzyme inhibitor, MK886, protected K562 cells against the drug. Conversely, the 5-lipoxygenase product, 5-hydroperoxyeicosatetraenoic acid, enhanced the tamoxifen-induced apoptosis. Finally, tamoxifen altered also membrane properties of K562 cells. Copyright (C) 1998 Federation of European Biochemical Societies.

Original languageEnglish
Pages (from-to)421-424
Number of pages4
JournalFEBS Letters
Volume434
Issue number3
DOIs
Publication statusPublished - Sep 4 1998

Keywords

  • 5-Lipoxygenase
  • Apoptosis
  • Biomembrane
  • Cholesterol
  • Nitric oxide synthase

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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