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Cancer Research 67, 1282-1290, February 1, 2007. doi: 10.1158/0008-5472.CAN-06-3099
© 2007 American Association for Cancer Research
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Experimental Therapeutics, Molecular Targets, and Chemical Biology

Tamoxifen Induces Oxidative Stress and Mitochondrial Apoptosis via Stimulating Mitochondrial Nitric Oxide Synthase

Rafal R. Nazarewicz1, Woineshet J. Zenebe1, Arti Parihar1, Sarah K. Larson1, Enver Alidema1, Jiho Choi2 and Pedram Ghafourifar1

1 Vascular Surgery, Davis Heart and Lung Research Institute, and Institute of Mitochondrial Biology, Ohio State University Medical Center, Columbus, Ohio and 2 Department of Community Health and Family Medicine, University of Florida School of Medicine, Gainesville, Florida

Requests for reprints: Pedram Ghafourifar, 510 Davis Heart and Lung Research Institute, Ohio State University Medical Center, 473 West 12th Avenue, Columbus, OH 43210. Phone: 614-247-7373; E-mail: Pedram.Ghafourifar{at}osumc.edu.

Tamoxifen is an anticancer drug that induces oxidative stress and apoptosis via mitochondria-dependent and nitric oxide (NO)–dependent pathways. The present report shows that tamoxifen increases intramitochondrial ionized Ca2+ concentration and stimulates mitochondrial NO synthase (mtNOS) activity in the mitochondria from rat liver and human breast cancer MCF-7 cells. By stimulating mtNOS, tamoxifen hampers mitochondrial respiration, releases cytochrome c, elevates mitochondrial lipid peroxidation, increases protein tyrosine nitration of certain mitochondrial proteins, decreases the catalytic activity of succinyl-CoA:3-oxoacid CoA-transferase, and induces aggregation of mitochondria. The present report suggests a critical role for mtNOS in apoptosis induced by tamoxifen. [Cancer Res 2007;67(3):1282–90]




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
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Copyright © 2007 by the American Association for Cancer Research.