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J Biol Chem, Vol. 273, Issue 9, 5294-5299, February 27, 1998
From the We previously observed that glucose deprivation
induces cell death in multidrug-resistant human breast carcinoma cells
(MCF-7/ADR). As a follow up we wished to test the hypothesis that
metabolic oxidative stress was the causative process or at least the
link between causative processes behind the cytotoxicity. In the
studies described here, we demonstrate that mitogen-activated protein kinase (MAPK) was activated within 3 min of being in glucose-free medium and remained activated for 3 h. Glucose deprivation for 2-4 h also caused oxidative stress as evidenced by a 3-fold greater steady state concentration of oxidized glutathione and a 3-fold increase in pro-oxidant production. Glucose and glutamate treatment rapidly suppressed MAPK activation and rescued cells from cytotoxicity. Glutamate and the peroxide scavenger, pyruvate, rescued the cells from
cell killing as well as suppressed pro-oxidant production. In addition
the thiol antioxidant, N-acetyl-L-cysteine,
rescued cells from glucose deprivation-induced cytotoxicity and
suppressed MAPK activation. These results suggest that glucose
deprivation-induced cytotoxicity and alterations in MAPK signal
transduction are mediated by oxidative stress in MCF-7/ADR. These
results also support the speculation that a common mechanism of glucose
deprivation-induced cytotoxicity in mammalian cells may involve
metabolic oxidative stress.
Glucose Deprivation-induced Cytotoxicity and Alterations in
Mitogen-activated Protein Kinase Activation Are Mediated by Oxidative
Stress in Multidrug-resistant Human Breast Carcinoma Cells
,,,
,, and
Department of Radiation Oncology and the
¶ Department of Clinical Pathology, William Beaumont Hospital,
Royal Oak, Michigan 48073 and the Section of Cancer Biology,
Radiation Oncology Center, Washington University School of
Medicine, St. Louis, Missouri 63108
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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