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DNA oxidation induced by cyclooxygenase-2

D Nikolic1, R B van Breemen

  • 1Department of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, University of Illinois at Chicago, 833 South Wood Street, Chicago, IL 60612-7231, USA.

Insights

Cyclooxygenase-2 (COX-2) overexpression in tumors may cause DNA oxidation via reactive oxygen species. Inhibiting COX-2 or using antioxidants can prevent this damage, suggesting a role in cancer prevention.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • The inducible cyclooxygenase, COX-2, is overexpressed in various cancers, including colon and prostate.
  • COX-2 inhibition shows potential for cancer prevention.
  • COX-2 reactions generate reactive oxygen radicals, potentially damaging macromolecules.

Purpose of the Study:

  • To investigate if DNA and nucleosides are oxidized during cyclooxygenase reactions.
  • To determine the role of COX-2 in DNA oxidation.

Main Methods:

  • Incubation of DNA or nucleosides with COX-2 and arachidonic acid.
  • Measurement of 8-oxo-2'-deoxyguanosine as a marker of DNA oxidation.
  • Testing the effects of COX-2 inhibitors and antioxidants.

Main Results:

  • A significant increase in 8-oxo-2'-deoxyguanosine was observed when DNA/nucleosides were incubated with COX-2 and arachidonic acid.
  • The oxidation was enzyme-dependent and could be blocked by COX-2 inhibitors and antioxidants.
  • Peroxyl radicals or other oxidized species formed during arachidonic acid conversion are likely responsible.

Conclusions:

  • COX-2 activity can lead to DNA oxidation.
  • Overexpression of COX-2 in inflammatory conditions may increase DNA damage and mutation risk.
  • COX-2 inhibition and antioxidant use could be strategies for cancer prevention by mitigating DNA oxidation.

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