Age-Related Loss of the DNA Repair Response Following Exposure to Oxidative Stress

Young (4- to 6-month-old) and aged (24- to 28-month-old) mice were exposed to 2-nitropropane (2-NP), a DNA oxidizing agent, and the ability to induce DNA polymerase β (β-pol) and AP endonuclease (APE) was determined. In contrast to the inducibility of these gene products in response to oxidative dam...

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Bibliographic Details
Published in:The journals of gerontology. Series A, Biological sciences and medical sciences Biological sciences and medical sciences, 2006-05, Vol.61 (5), p.427-434
Main Authors: Cabelof, Diane C., Raffoul, Julian J., Ge, Yubin, Van Remmen, Holly, Matherly, Larry H., Heydari, Ahmad R.
Format: Article
Language:English
Subjects:
Age
Age Factors
Aging - physiology
Analysis of Variance
Animals
Blotting, Western
Disease Models, Animal
DNA Damage
DNA repair
DNA Repair - drug effects
DNA Repair - physiology
DNA-(Apurinic or Apyrimidinic Site) Lyase - drug effects
DNA-(Apurinic or Apyrimidinic Site) Lyase - metabolism
Genomics
Male
Mice
Mice, Inbred Strains
Mutation
Nitroparaffins - pharmacology
Oxidative Stress
Probability
Propane - analogs & derivatives
Propane - pharmacology
Reference Values
Reverse Transcriptase Polymerase Chain Reaction
Risk Factors
Rodents
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Summary:Young (4- to 6-month-old) and aged (24- to 28-month-old) mice were exposed to 2-nitropropane (2-NP), a DNA oxidizing agent, and the ability to induce DNA polymerase β (β-pol) and AP endonuclease (APE) was determined. In contrast to the inducibility of these gene products in response to oxidative damage in young mice, aged mice showed a lack of inducibility of β-pol and APE. APE protein level and endonuclease activity were both reduced 40% (p
ISSN:1079-5006
1758-535X
DOI:10.1093/gerona/61.5.427