Oxidative DNA damage in the aging mouse brain
Identifieur interne : 004C96 ( Main/Exploration ); précédent : 004C95; suivant : 004C97Oxidative DNA damage in the aging mouse brain
Auteurs : Fernando Cardozo-Pelaez [États-Unis] ; Shijie Song [États-Unis] ; Anand Parthasarathy [États-Unis] ; Christopher Hazzi [États-Unis] ; Kamatham Naidu [États-Unis] ; Juan Sanchez-Ramos [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 1999-11.
English descriptors
Abstract
The brain exhibits regional vulnerabilities to many insults, and age itself has differential effects on neuronal populations as exemplified by the age‐dependent loss of dopaminergic neurons in the nigrostriatal system. We hypothesized that oxidative damage to DNA was more likely to occur in the nigrostriatal system which undergoes significant neurochemical and functional changes with age. To test this hypothesis, oxidative damage to DNA, indicated by levels of 8‐hydroxy‐2′‐deoxyguanosine (oxo8dG), was measured in pons‐medulla (PM), midbrain (MB), caudate‐putamen (CP), hippocampus (HP), cerebellum (CB), and cerebral cortex (CX) at 3, 18, and 34 months of age in C57/bl mice. Steady‐state levels of oxo8dG increased significantly with age in MB, CP, and CB, but not in PM, HP, or CX. Manganese superoxide dismutase (MnSOD) activity decreased with age in MB, CP, and HP, but not in PM, CB, or CX. Regional activities of Cu/Zn superoxide dismutase (Cu/Zn SOD) and glutathione peroxidase (Glut Px) did not change significantly with age. Concomitant with the regional alterations in DNA damage, there was a significant age‐dependent decline in locomotor activity, motor coordination, and striatal dopamine content especially during the interval between 18 and 34 months. In conclusion, oxyradical‐associated damage to DNA did not accumulate uniformly across brain regions with age and was highest in brain regions that subserve spontaneous locomotor activity and motor coordination.
Url:
DOI: 10.1002/1531-8257(199911)14:6<972::AID-MDS1010>3.0.CO;2-0
Affiliations:
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="1999-11">1999-11</date><biblScope unit="vol">14</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="972">972</biblScope><biblScope unit="page" to="980">980</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">68A6803B2A7D65E75EF99362A46221F1638EF57B</idno><idno type="DOI">10.1002/1531-8257(199911)14:6<972::AID-MDS1010>3.0.CO;2-0</idno><idno type="ArticleID">MDS1010</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>8‐hydroxy‐2′deoxyguanosine</term><term>Aging</term><term>DNA damage</term><term>Dopamine</term><term>Locomotor activity</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The brain exhibits regional vulnerabilities to many insults, and age itself has differential effects on neuronal populations as exemplified by the age‐dependent loss of dopaminergic neurons in the nigrostriatal system. We hypothesized that oxidative damage to DNA was more likely to occur in the nigrostriatal system which undergoes significant neurochemical and functional changes with age. To test this hypothesis, oxidative damage to DNA, indicated by levels of 8‐hydroxy‐2′‐deoxyguanosine (oxo8dG), was measured in pons‐medulla (PM), midbrain (MB), caudate‐putamen (CP), hippocampus (HP), cerebellum (CB), and cerebral cortex (CX) at 3, 18, and 34 months of age in C57/bl mice. Steady‐state levels of oxo8dG increased significantly with age in MB, CP, and CB, but not in PM, HP, or CX. Manganese superoxide dismutase (MnSOD) activity decreased with age in MB, CP, and HP, but not in PM, CB, or CX. Regional activities of Cu/Zn superoxide dismutase (Cu/Zn SOD) and glutathione peroxidase (Glut Px) did not change significantly with age. Concomitant with the regional alterations in DNA damage, there was a significant age‐dependent decline in locomotor activity, motor coordination, and striatal dopamine content especially during the interval between 18 and 34 months. In conclusion, oxyradical‐associated damage to DNA did not accumulate uniformly across brain regions with age and was highest in brain regions that subserve spontaneous locomotor activity and motor coordination.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Floride</li></region><settlement><li>Tampa</li></settlement><orgName><li>Université de Floride du Sud</li></orgName></list><tree><country name="États-Unis"><region name="Floride"><name sortKey="Cardozo Elaez, Fernando" sort="Cardozo Elaez, Fernando" uniqKey="Cardozo Elaez F" first="Fernando" last="Cardozo-Pelaez">Fernando Cardozo-Pelaez</name></region><name sortKey="Hazzi, Christopher" sort="Hazzi, Christopher" uniqKey="Hazzi C" first="Christopher" last="Hazzi">Christopher Hazzi</name><name sortKey="Naidu, Kamatham" sort="Naidu, Kamatham" uniqKey="Naidu K" first="Kamatham" last="Naidu">Kamatham Naidu</name><name sortKey="Parthasarathy, Anand" sort="Parthasarathy, Anand" uniqKey="Parthasarathy A" first="Anand" last="Parthasarathy">Anand Parthasarathy</name><name sortKey="Sanchez Amos, Juan" sort="Sanchez Amos, Juan" uniqKey="Sanchez Amos J" first="Juan" last="Sanchez-Ramos">Juan Sanchez-Ramos</name><name sortKey="Song, Shijie" sort="Song, Shijie" uniqKey="Song S" first="Shijie" last="Song">Shijie Song</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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