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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
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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

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Role of oxidative stress and DNA damage in human carcinogenesis

Thomas B Kryston1, Anastassiya B Georgiev, Polycarpos Pissis

  • 1Department of Biology, Thomas Harriot College of Arts and Sciences, East Carolina University, Greenville, NC 27858, USA.

Mutation Research
|January 11, 2011
PubMed

Insights

Cells face daily oxidative stress from free radicals, triggering DNA damage. This review explores oxidative stress, DNA damage, and their role in human cancer development and potential as biomarkers.

Area of Science:

  • Molecular Biology
  • Biochemistry
  • Oncology

Background:

  • Cells are constantly exposed to endogenous and exogenous oxidative stress and free radicals.
  • Cells possess defense mechanisms including antioxidants like glutathione (GSH), vitamins C and E, and enzymes such as catalase and superoxide dismutase.
  • Oxidative stress can lead to various DNA lesions, from base lesions and single-strand breaks (SSBs) to complex double-strand breaks (DSBs) and oxidatively generated clustered DNA lesions (OCDLs).

Purpose of the Study:

  • To review the current understanding of intracellular oxidative stress and DNA damage mechanisms in human cancer.
  • To discuss the involvement of these factors in human malignancy evolution.
  • To explore the potential of oxidative stress and DNA damage as cancer biomarkers.

Main Methods:

  • Literature review of current knowledge on oxidative stress and DNA damage.
  • Analysis of mechanisms linking oxidative stress, DNA damage, and cancer progression.
  • Discussion of methodologies for measuring DNA lesions and associated artifacts.

Main Results:

  • Oxidative stress induces a spectrum of DNA damage, including SSBs, DSBs, and OCDLs.
  • Accumulation of unrepaired or misrepaired DNA damage can cause mutagenesis and cellular transformation.
  • Deficiencies in DNA repair or apoptotic pathways exacerbate the risk of cancer development.

Conclusions:

  • Intracellular oxidative stress and subsequent DNA damage are implicated in human cancer evolution.
  • Oxidative DNA damage and repair mechanisms may serve as valuable cancer biomarkers.
  • Methodological considerations are crucial for accurate measurement of oxidative DNA lesions.

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