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Collaborations with Miral Dizdaroglu: expanding on connections between oxidative DNA damage and aging and disease

Vilhelm A Bohr1

  • 1Department of ICMM, University of Copenhagen, Copenhagen, Denmark.

International Journal of Radiation Biology
|August 10, 2026
PubMed
Abstract

Insights

This study reveals oxidative DNA damage extends beyond 8-oxo-Gua, implicating Base Excision Repair defects in aging and neurodegeneration. A multi-lesion approach is crucial for understanding disease links.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Genetics

Background:

  • Oxidative stress is implicated in aging and diseases like neurodegeneration and cancer.
  • Understanding DNA damage and repair mechanisms is crucial for disease pathology.
  • The role of specific DNA lesions beyond 8-oxo-Gua requires further investigation.

Purpose of the Study:

  • To investigate oxidative DNA damage and repair mechanisms.
  • To identify endogenous DNA lesions like FapyGua and FapyAde.
  • To determine the biological significance and distribution of these lesions in nuclear and mitochondrial DNA.

Main Methods:

  • Gas Chromatography/Mass Spectrometry (GC/MS) assays were employed.
  • Identification of key DNA repair glycosylases (OGG1, NTH1) and stimulating proteins (CSB).
  • Analysis of DNA repair deficiencies in patients with Cockayne syndrome (CSB) and Xeroderma pigmentosum (XPA).

Main Results:

  • OGG1 and NTH1 are primary glycosylases for formamidopyrimidines; CSB protein stimulates NEIL1.
  • CSB and XPA patients exhibit deficiencies in repairing specific oxidative lesions, linked to premature aging.
  • Reduced hOGG1 expression in lung cancer correlates with elevated 8-oxo-Gua; nuclear and mitochondrial DNA damage induction is similar.

Conclusions:

  • Oxidative DNA damage involves lesions beyond 8-oxo-Gua.
  • Base Excision Repair (BER) defects are central to cancer and neurodegeneration.
  • A multi-lesion approach is essential for understanding oxidative stress and disease links.
Keywords:
Cockayne syndromeOxidative DNA damageagingbase excision repairformamidopyrimidinesmitochondrial DNA

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