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Related Experiment Videos

Cyclooxygenase-2-mediated DNA damage.

Seon Hwa Lee1, Michelle V Williams, Raymond N Dubois

  • 1Center for Cancer Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6160, USA.

The Journal of Biological Chemistry
|June 21, 2005
PubMed
Summary
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Cyclooxygenase-2 (COX-2) activity leads to DNA damage via lipid peroxidation, not prostaglandin formation. Inhibiting COX-2-mediated lipid hydroperoxides may offer a new chemoprevention strategy against tumorigenesis.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Oxidative stress is implicated in tumorigenesis.
  • Cyclooxygenase-2 (COX-2) plays a role in cellular processes.
  • Lipid peroxidation can lead to DNA damage.

Purpose of the Study:

  • To investigate the role of COX-2 in DNA damage through lipid peroxidation.
  • To explore the mechanism of DNA adduct formation.
  • To evaluate potential chemoprevention strategies targeting COX-2 pathways.

Main Methods:

  • Utilized rat intestinal epithelial cells (RIES cells) expressing COX-2 as an oxidative stress model.
  • Employed targeted lipidomics to identify lipid mediators.
  • Analyzed DNA adduct formation using techniques like identifying heptanone-etheno-2'-deoxyguanosine.

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  • Investigated the effects of vitamin C, NS-398 (COX-2 inhibitor), and aspirin.

    • Main Results:

    • 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE) and its hydroperoxide (15(S)-HPETE) were major lipids formed.
    • 15(S)-HPETE decomposed to 4-oxo-2(E)-nonenal, forming the DNA adduct heptanone-etheno-2'-deoxyguanosine.
    • Vitamin C increased adduct levels, while NS-398 showed protective effects.
    • Aspirin treatment led to 15(R)-HETE formation but not increased adducts, suggesting a COX-2 specific mechanism.

    Conclusions:

    • COX-2-mediated lipid peroxidation, rather than prostaglandin synthesis, is a potential mechanism for DNA adduct formation and tumorigenesis.
    • Inhibiting COX-2-mediated lipid hydroperoxide formation presents a novel therapeutic avenue for chemoprevention.