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Research Article Free access | 10.1172/JCI3437

Role of oxygen radicals generated by NADPH oxidase in apoptosis induced in human leukemia cells.

W Hiraoka, N Vazquez, W Nieves-Neira, S J Chanock, and Y Pommier

Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, Maryland 20892, USA.

Find articles by Hiraoka, W. in: JCI | PubMed | Google Scholar

Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, Maryland 20892, USA.

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Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, Maryland 20892, USA.

Find articles by Nieves-Neira, W. in: JCI | PubMed | Google Scholar

Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, Maryland 20892, USA.

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Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, Maryland 20892, USA.

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Published December 1, 1998 - More info

Published in Volume 102, Issue 11 on December 1, 1998
J Clin Invest. 1998;102(11):1961–1968. https://doi.org/10.1172/JCI3437.
© 1998 The American Society for Clinical Investigation
Published December 1, 1998 - Version history
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Abstract

We have used a human leukemia cell line that, after homologous recombination knockout of the gp91-phox subunit of the phagocyte respiratory-burst oxidase cytochrome b-558, mimics chronic granulomatous disease (X-CGD) to study the role of oxygen radicals in apoptosis. Camptothecin (CPT), a topoisomerase I inhibitor, induced significantly more apoptosis in PLB-985 cells than in X-CGD cells. Sensitivity to CPT was enhanced after neutrophilic differentiation, but was lost after monocytic differentiation. No difference between the two cell lines was observed after treatment with other apoptosis inducers, including etoposide, ultraviolet radiation, ionizing radiation, hydrogen peroxide, or 7-hydroxystaurosporine. After granulocytic differentiation of both cell lines, CPT still induced apoptosis, suggesting independence from replication in fully differentiated and growth-arrested cells. Pyrrolidine dithiocarbamate (an antioxidant inhibitor of NF-kappaB) and catalase partially inhibited CPT-induced DNA fragmentation in granulocytic-differentiated PLB-985 cells, but had no effect in X-CGD cells. Flow cytometry analysis revealed that reactive oxygen intermediates were generated in CPT-treated PLB-985 cells. These data indicate that oxygen radicals generated by NADPH oxidase may contribute directly or indirectly to CPT-induced apoptosis in human leukemia and in neutrophilic-differentiated cells.

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