Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Oxidative DNA damage processing and changes with aging.

V Bohr1, R M Anson, S Mazur

  • 1Laboratory of Molecular Genetics, National Institute on Aging, NIH, Baltimore, MD 21224, USA.

Toxicology Letters
|February 18, 1999
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Endovascular Repair of an Iliac Arteriovenous Fistula in a 30-Year-Old Female Patient with Suspected Severe Cardiac Insufficiency: A Case Report.

Cardiology and therapy·2022
Same author

Comparison of mouse, rat and rabbit models for adipose - Derived stem cells (ASC) research.

Current research in translational medicine·2020
Same author

[Therapeutic advances in cystic fibrosis in 2014].

Revue de pneumologie clinique·2015
Same author

Photodynamic diagnosis (PDD) and photodynamic therapy (PDT) in dermatology: "How we do it".

Photodiagnosis and photodynamic therapy·2014
Same author

Mitochondria, oxidative DNA damage, and aging.

Journal of the American Aging Association·2013
Same author

Cells deficient in the base excision repair protein, DNA polymerase beta, are hypersensitive to oxaliplatin chemotherapy.

Oncogene·2009
Same journal

LEF1 regulated CTHRC1 Promotes Silica-Induced Pulmonary Fibrosis through CD44-Dependent Signaling.

Toxicology letters·2026
Same journal

hERG Channel Blockade and Additive Interactions of Magnolol and Honokiol from Magnolia Species.

Toxicology letters·2026
Same journal

Evaluation of dose-dependent hematotoxic effects of celastrol on human blood cells in vitro.

Toxicology letters·2026
Same journal

Environmental pharmaceutical and antibiotic mixtures: An exposomics-guided framework for mechanistic toxicology.

Toxicology letters·2026
Same journal

Size- and morphology-dependent cytotoxicity of metal-organic frameworks: Deciphering the structure-toxicity relationship.

Toxicology letters·2026
Same journal

Steroidogenesis suppression in H295R cells by 1,3-disubstituted ureas: A potential off-target effect of some sEH inhibitors.

Toxicology letters·2026
See all related articles

Oxidative stress damages DNA, leading to aging and cancer. Organisms possess DNA repair mechanisms, but deficiencies in nuclear DNA repair, as seen in Cockayne syndrome, may cause premature aging.

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Organisms face constant oxidative stress from internal and external sources.
  • Oxidative stress causes modifications in proteins, lipids, and DNA, with DNA damage being a primary concern due to its link to mutations, cancer, and aging.
  • Oxidative DNA lesions accumulate with age, predominantly in mitochondrial DNA.

Purpose of the Study:

  • To investigate the complex DNA repair mechanisms for oxidative damage.
  • To differentiate and measure DNA repair processes in both nuclear and mitochondrial DNA.
  • To explore the role of DNA repair deficiencies in premature aging disorders like Cockayne syndrome.

Main Methods:

  • Utilized diverse experimental approaches to study DNA repair pathways.

Related Experiment Videos

  • Examined the repair of various oxidative DNA lesions.
  • Quantified different stages of DNA repair processes.
  • Measured DNA damage processing distinctly in nuclear and mitochondrial DNA.

    • Main Results:

    • Mitochondria possess efficient DNA repair mechanisms for oxidative damage, challenging previous assumptions.
    • Identified potential deficiencies in nuclear DNA repair of oxidative damage in Cockayne syndrome.
    • Linked these repair deficiencies to the premature aging phenotype observed in Cockayne syndrome.

    Conclusions:

    • Mitochondrial DNA repair is more robust than previously thought.
    • Deficiencies in nuclear DNA repair of oxidative stress are implicated in premature aging disorders.
    • Further research into DNA repair pathways is crucial for understanding aging and disease.