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JNCI Journal of the National Cancer Institute 2006 98(4):223-225; doi:10.1093/jnci/djj065
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© The Author 2006. Published by Oxford University Press.

EDITORIAL

Redox Modulation of Chemotherapy-Induced Tumor Cell Killing and Normal Tissue Toxicity

James H. Doroshow

Correspondence to: James H. Doroshow, MD, Division of Cancer Treatment and Diagnosis, National Cancer Institute, 31 Center Dr., Bldg. 31, Rm. 3A44, National Institutes of Health, Bethesda, MD 20892 (e-mail: doroshoj@mail.nih.gov).

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The traditional view of intracellular oxidation–reduction, or redox, balance in epithelial cells, which is more than three decades old (1), emphasizes a dynamic equilibrium between the production of reactive oxygen species (ROS; these include superoxide anion, O2–; hydrogen peroxide, H2O2; and chemical species with the characteristics of the hydroxyl radical, bulletOH) by a variety of flavin dehydrogenases that occupy essentially every cellular compartment, and the detoxification of these species by a broad range of antioxidant enzymes and related small molecules (2). ROS are produced by the mitochondrial electron transport chain during the course of cellular respiration, by cytochrome P450–related components of microsomes (3), and, in many human tumors, by the recently described family of membrane-bound NADPH oxidases that possess a high degree of homology with components of the NADPH . . . [Full Text of this Article]


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