Prooxidant States and Tumor Promotion

There is convincing evidence that cellular prooxidant states--that is, increased concentrations of active oxygen and organic peroxides and radicals--can promote initiated cells to neoplastic growth. Prooxidant states can be caused by different classes of agents, including hyperbaric oxygen, radiatio...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1985-01, Vol.227 (4685), p.375-381
Main Author: Cerutti, Peter A.
Format: Article
Language:English
Subjects:
Animals
Antioxidants
Antioxidants - pharmacology
Biological and medical sciences
Cancer
Cancer research
Carcinogenesis
Carcinogenesis, carcinogens and anticarcinogens
Carcinogens - metabolism
Carcinogens - pharmacology
Cations - metabolism
Cell Differentiation
Cell Division
Cell Line
Cell Membrane - physiology
Cell Transformation, Neoplastic
Chromosome Aberrations
Chromosomes - drug effects
Cytochrome P-450 Enzyme System - metabolism
DNA - metabolism
DNA damage
Electron Transport
Embryonic cells
Epidermal cells
Fibroblasts
Gene expression
Gene Expression Regulation
General aspects
Genetic research
Humans
Hydrogen Peroxide - metabolism
Hydroxides - metabolism
Hydroxyl Radical
Lipid Peroxides - metabolism
Lymphocytes
Medical sciences
Microbodies - metabolism
Mutation
Neoplasms - chemically induced
Observations
Oncology, Experimental
Oxidation-Reduction
Oxygen - metabolism
Oxygen - physiology
Peroxides
Poly Adenosine Diphosphate Ribose - metabolism
Reactive oxygen species
Singlet Oxygen
Sulfhydryl Compounds - physiology
Superoxides - metabolism
Tumors
Ultraviolet Rays
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Summary:There is convincing evidence that cellular prooxidant states--that is, increased concentrations of active oxygen and organic peroxides and radicals--can promote initiated cells to neoplastic growth. Prooxidant states can be caused by different classes of agents, including hyperbaric oxygen, radiation, xenobiotic metabolites and Fenton-type reagents, modulators of the cytochrome P-450 electron-transport chain, peroxisome proliferators, inhibitors of the antioxidant defense, and membrane-active agents. Many of these agents are promoters or complete carcinogens. They cause chromosomal damage by indirect action, but the role of this damage in carcinogenesis remains unclear. Prooxidant states can be prevented or suppressed by the enzymes of the cellular antioxidant defense and low molecular weight scavenger molecules, and many antioxidants are antipromoters and anticarcinogens. Finally, prooxidant states may modulate the expression of a family of prooxidant genes, which are related to cell growth and differentiation, by inducing alterations in DNA structure or by epigenetic mechanisms, for example, by polyadenosine diphosphate--ribosylation of chromosomal proteins.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.2981433