Abstract
Chemical carcinogenesis follows a multistep process involving both mutation and increased cell proliferation. Oxidative stress can occur through overproduction of reactive oxygen and nitrogen species through either endogenous or exogenous insults. Important to carcinogenesis, the unregulated or prolonged production of cellular oxidants has been linked to mutation (induced by oxidant-induced DNA damage), as well as modification of gene expression. In particular, signal transduction pathways, including AP-1 and NFκB, are known to be activated by reactive oxygen species, and they lead to the transcription of genes involved in cell growth regulatory pathways. This review examines the evidence of cellular oxidants' involvement in the carcinogenesis process, and focuses on the mechanisms for production, cellular damage produced, and the role of signaling cascades by reactive oxygen species.
Keywords
CarcinogenesisReactive oxygen speciesOxidative stressDNA damageSignal transductionCell biologyEndogenyTranscription factorReactive nitrogen speciesChemistryMutationBiologyBiochemistryDNAGene
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Publication Info
- Year
- 2004
- Type
- review
- Volume
- 44
- Issue
- 1
- Pages
- 239-267
- Citations
- 1512
- Access
- Closed
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Cite This
James E. Klaunig,
Lisa M. Kamendulis
(2004).
The Role of Oxidative Stress in Carcinogenesis.
The Annual Review of Pharmacology and Toxicology
, 44
(1)
, 239-267.
https://doi.org/10.1146/annurev.pharmtox.44.101802.121851
Identifiers
- DOI
- 10.1146/annurev.pharmtox.44.101802.121851