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

doi:10.1016/S0014-5793(98)01026-6

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 journal › Article › peer-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 language	English
Pages (from-to)	421-424
Number of pages	4
Journal	FEBS Letters
Volume	434
Issue number	3
DOIs	https://doi.org/10.1016/S0014-5793(98)01026-6
Publication status	Published - Sep 4 1998

Keywords

5-Lipoxygenase
Apoptosis
Biomembrane
Cholesterol
Nitric oxide synthase

ASJC Scopus subject areas

Biochemistry
Biophysics
Molecular Biology

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

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.",

keywords = "5-Lipoxygenase, Apoptosis, Biomembrane, Cholesterol, Nitric oxide synthase",

author = "Mauro Maccarrone and Cristina Fantini and Marco Ranalli and Gerry Melino and Agr{\`o}, {Alessandro Finazzi}",

year = "1998",

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T1 - Activation of nitric oxide synthase is involved in tamoxifen-induced apoptosis of human erythroleukemia K562 cells

AU - Maccarrone, Mauro

AU - Fantini, Cristina

AU - Ranalli, Marco

AU - Melino, Gerry

AU - Agrò, Alessandro Finazzi

PY - 1998/9/4

Y1 - 1998/9/4

N2 - 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.

AB - 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.

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KW - Cholesterol

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