The role of oxidative stress in amyotrophic lateral sclerosis and Parkinson's disease.
Identifieur interne : 000A40 ( PubMed/Corpus ); précédent : 000A39; suivant : 000A41The role of oxidative stress in amyotrophic lateral sclerosis and Parkinson's disease.
Auteurs : Athan Baillet ; Vanessa Chanteperdrix ; Candice Trocmé ; Pierre Casez ; Catherine Garrel ; Gérard BessonSource :
- Neurochemical research [ 1573-6903 ] ; 2010.
English descriptors
- KwdEn :
- Adult, Age Factors, Amyotrophic Lateral Sclerosis (metabolism), Antioxidants (metabolism), Biomarkers (metabolism), Female, Glutathione Peroxidase (metabolism), Humans, Male, Middle Aged, Multivariate Analysis, Oxidative Stress, Parkinson Disease (metabolism), Sex Factors, Superoxide Dismutase (metabolism), Trace Elements (metabolism).
- MESH :
- chemical , metabolism : Antioxidants, Biomarkers, Glutathione Peroxidase, Superoxide Dismutase, Trace Elements.
- metabolism : Amyotrophic Lateral Sclerosis, Parkinson Disease.
- Adult, Age Factors, Female, Humans, Male, Middle Aged, Multivariate Analysis, Oxidative Stress, Sex Factors.
Abstract
We examined oxidative stress markers of 31 patients suffering from ALS, 24 patients suffering from PD and 30 healthy subjects were included. We determined the plasma levels of lipid peroxidation (malondialdehyde, MDA), of protein oxidative lesions (plasma glutathione, carbonyls and thiols) and the activity of antioxidant enzymes i.e. erythrocyte Cu,Zn-Superoxide dismutase (SOD), Glutathione peroxidase (GSH-Px) and catalase. MDA and thiols were significantly different in both neurodegenerative diseases versus control population. A trend for an enhancement of oxidized glutathione was noted in ALS patients. Univariate analysis showed that SOD activity was significantly decreased in ALS and GSH-Px activity was decreased in PD. After adjusting for demographic parameters and enzyme cofactors, we could emphasize a compensatory increase of SOD activity in PD. Different antioxidant systems were not involved in the same way in ALS and PD, suggesting that oxidative stress may be a cause rather than a consequence of the neuronal death.
DOI: 10.1007/s11064-010-0212-5
PubMed: 20535556
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pubmed:20535556Le document en format XML
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<author><name sortKey="Trocme, Candice" sort="Trocme, Candice" uniqKey="Trocme C" first="Candice" last="Trocmé">Candice Trocmé</name>
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<author><name sortKey="Casez, Pierre" sort="Casez, Pierre" uniqKey="Casez P" first="Pierre" last="Casez">Pierre Casez</name>
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<author><name sortKey="Garrel, Catherine" sort="Garrel, Catherine" uniqKey="Garrel C" first="Catherine" last="Garrel">Catherine Garrel</name>
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<front><div type="abstract" xml:lang="en">We examined oxidative stress markers of 31 patients suffering from ALS, 24 patients suffering from PD and 30 healthy subjects were included. We determined the plasma levels of lipid peroxidation (malondialdehyde, MDA), of protein oxidative lesions (plasma glutathione, carbonyls and thiols) and the activity of antioxidant enzymes i.e. erythrocyte Cu,Zn-Superoxide dismutase (SOD), Glutathione peroxidase (GSH-Px) and catalase. MDA and thiols were significantly different in both neurodegenerative diseases versus control population. A trend for an enhancement of oxidized glutathione was noted in ALS patients. Univariate analysis showed that SOD activity was significantly decreased in ALS and GSH-Px activity was decreased in PD. After adjusting for demographic parameters and enzyme cofactors, we could emphasize a compensatory increase of SOD activity in PD. Different antioxidant systems were not involved in the same way in ALS and PD, suggesting that oxidative stress may be a cause rather than a consequence of the neuronal death.</div>
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<Abstract><AbstractText>We examined oxidative stress markers of 31 patients suffering from ALS, 24 patients suffering from PD and 30 healthy subjects were included. We determined the plasma levels of lipid peroxidation (malondialdehyde, MDA), of protein oxidative lesions (plasma glutathione, carbonyls and thiols) and the activity of antioxidant enzymes i.e. erythrocyte Cu,Zn-Superoxide dismutase (SOD), Glutathione peroxidase (GSH-Px) and catalase. MDA and thiols were significantly different in both neurodegenerative diseases versus control population. A trend for an enhancement of oxidized glutathione was noted in ALS patients. Univariate analysis showed that SOD activity was significantly decreased in ALS and GSH-Px activity was decreased in PD. After adjusting for demographic parameters and enzyme cofactors, we could emphasize a compensatory increase of SOD activity in PD. Different antioxidant systems were not involved in the same way in ALS and PD, suggesting that oxidative stress may be a cause rather than a consequence of the neuronal death.</AbstractText>
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