Oxidatively damaged DNA in aging dyslipidemic ApoE-/- and wild-type mice.

2.50
Hdl Handle:
http://hdl.handle.net/10146/24120
Title:
Oxidatively damaged DNA in aging dyslipidemic ApoE-/- and wild-type mice.
Authors:
Folkmann, Janne Kjaersgaard; Loft, Steffen; Moller, Peter
Abstract:
The free radical theory of aging depicts an accumulation of cellular oxidatively damaged DNA. In this study, we investigated this theory in mice with knocked-out apolipoprotein E gene (ApoE(-/-)), which develops atherosclerosis and wild-type counterparts. The level of oxidatively damaged DNA was investigated as strand breaks, endonuclease III- and formamidopyrimidine DNA glycosylase-sensitive sites by the comet assay. The level of DNA damage was mainly increased with age in the liver of ApoE(-/-) mice, whereas no increase was observed in the aorta or lung of the mice. This suggests that the accumulation of oxidized DNA in the liver of dyslipidemic ApoE(-/-) mice could be secondary to dysfunction of the lipid metabolism. Visually, the aortas of the ApoE(-/-) mice were clearly atherosclerotic as indicated by rigid texture and yellowish in color. However, the unaltered levels of oxidized DNA in severely atherosclerotic aortas of old ( approximately 70 weeks) ApoE(-/-) mice indicate that oxidative stress may not be a generalized phenomenon, but rather related locally to the individual plaques. In conclusion, the results of this study suggest that dyslipidemic ApoE(-/-) mice suffer from hepatic oxidative stress in terms of oxidized DNA, and this effect could be due to the dysfunction of lipid metabolism.
Citation:
Mutagenesis 2007, 22 (2):105-110
Journal:
Mutagenesis
Issue Date:
Mar-2007
URI:
http://hdl.handle.net/10146/24120
DOI:
10.1093/mutage/gel059
PubMed ID:
17234687
Additional Links:
http://mutage.oxfordjournals.org/cgi/content/full/22/2/105
Type:
Article
Language:
en
ISSN:
0267-8357
Sponsors:
This work was partly supported by Environmental Cancer Risk, Nutrition and Individual Susceptibility, a network of excellence operating within the European Union 6th Framework Program, Priority 5: "Food Quality and Safety" (Contract No. 513943) and the Danish Research Councils.
Appears in Collections:
Articles

Full metadata record

DC FieldValue Language
dc.contributor.authorFolkmann, Janne Kjaersgaard-
dc.contributor.authorLoft, Steffen-
dc.contributor.authorMoller, Peter-
dc.date.accessioned2008-04-24T11:33:50Z-
dc.date.available2008-04-24T11:33:50Z-
dc.date.issued2007-03-
dc.identifier.citationMutagenesis 2007, 22 (2):105-110en
dc.identifier.issn0267-8357-
dc.identifier.pmid17234687-
dc.identifier.doi10.1093/mutage/gel059-
dc.identifier.urihttp://hdl.handle.net/10146/24120-
dc.description.abstractThe free radical theory of aging depicts an accumulation of cellular oxidatively damaged DNA. In this study, we investigated this theory in mice with knocked-out apolipoprotein E gene (ApoE(-/-)), which develops atherosclerosis and wild-type counterparts. The level of oxidatively damaged DNA was investigated as strand breaks, endonuclease III- and formamidopyrimidine DNA glycosylase-sensitive sites by the comet assay. The level of DNA damage was mainly increased with age in the liver of ApoE(-/-) mice, whereas no increase was observed in the aorta or lung of the mice. This suggests that the accumulation of oxidized DNA in the liver of dyslipidemic ApoE(-/-) mice could be secondary to dysfunction of the lipid metabolism. Visually, the aortas of the ApoE(-/-) mice were clearly atherosclerotic as indicated by rigid texture and yellowish in color. However, the unaltered levels of oxidized DNA in severely atherosclerotic aortas of old ( approximately 70 weeks) ApoE(-/-) mice indicate that oxidative stress may not be a generalized phenomenon, but rather related locally to the individual plaques. In conclusion, the results of this study suggest that dyslipidemic ApoE(-/-) mice suffer from hepatic oxidative stress in terms of oxidized DNA, and this effect could be due to the dysfunction of lipid metabolism.en
dc.description.sponsorshipThis work was partly supported by Environmental Cancer Risk, Nutrition and Individual Susceptibility, a network of excellence operating within the European Union 6th Framework Program, Priority 5: "Food Quality and Safety" (Contract No. 513943) and the Danish Research Councils.en
dc.language.isoenen
dc.relation.urlhttp://mutage.oxfordjournals.org/cgi/content/full/22/2/105en
dc.subject.meshAging-
dc.subject.meshAnimals-
dc.subject.meshAorta-
dc.subject.meshApolipoproteins E-
dc.subject.meshDNA Damage-
dc.subject.meshDNA Glycosylases-
dc.subject.meshDyslipidemias-
dc.subject.meshEndonucleases-
dc.subject.meshFemale-
dc.subject.meshLiver-
dc.subject.meshLung-
dc.subject.meshMice-
dc.subject.meshMice, Inbred C57BL-
dc.subject.meshOxidative Stress-
dc.titleOxidatively damaged DNA in aging dyslipidemic ApoE-/- and wild-type mice.en
dc.typeArticleen
dc.identifier.journalMutagenesisen

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