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Quantification of three DNA Lesions by Mass Spectrometry and Assessment of Their Levels in Tissues of Mice Exposed to Ambient Fine Particulate Matter
Published on: May 29, 2019
Oxidative stress and oxidative damage in carcinogenesis
James E Klaunig1, Lisa M Kamendulis, Barbara A Hocevar
1Indiana University School of Medicine, Indianapolis, IN 46202, USA. jklauni@iupui.edu
Toxicologic Pathology
|December 19, 2009
Summary
Reactive oxygen species (ROS) contribute to cancer development by damaging DNA and altering gene expression. Genetic variations in DNA repair and antioxidant genes may influence cancer susceptibility.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Carcinogenesis is a multistep process involving cellular mutations and clonal expansion.
- Chemical and physical agents can induce or modulate carcinogenesis, often via reactive oxygen species (ROS).
Purpose of the Study:
- To discuss the role of ROS in carcinogenesis.
- To explore how ROS-induced oxidative damage and altered gene expression contribute to cancer development.
- To examine the association between genetic variations in oxidative DNA repair and antioxidant genes and human cancer susceptibility.
Main Methods:
- Review of scientific literature on ROS, oxidative stress, and carcinogenesis.
- Analysis of signaling pathways (Nrf2, NF-kappaB) affected by ROS.
- Examination of evidence linking single nucleotide polymorphisms (SNPs) in relevant genes to cancer risk.
Main Results:
- ROS production is a key mechanism by which carcinogens induce cancer.
- Oxidative damage to macromolecules and altered gene expression driven by ROS signaling contribute to cancer progression.
- SNPs in oxidative DNA repair and antioxidant genes are associated with human cancer susceptibility.
Conclusions:
- ROS play a significant role in the multistep process of carcinogenesis.
- Understanding ROS biology and genetic factors is crucial for cancer prevention and treatment strategies.
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