Antiparkinsonian therapies and brain mitochondrial complex I activity
Identifieur interne : 002359 ( Main/Exploration ); précédent : 002358; suivant : 002360Antiparkinsonian therapies and brain mitochondrial complex I activity
Auteurs : Przedborski [États-Unis] ; Vernice Jackson-Lewis [États-Unis] ; Stanley Fahn [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 1995-05.
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Abstract
Alterations in complex I activity, one of the enzymatic units of the mitochondrial respiratory chain, have been demonstrated in different tissues from patients with Parkinson's disease (PD). Subsequently, we showed that the chronic administration of levodopa can cause alterations in mitochondrial respiratory chain activity in rats, which suggests that the observed deficit in complex I activity in PD might be, at least in part, related to chronic levodopa therapy. Our study assessed the in vitro effects of different antiparkinsonian agents on complex I activity in rat brain. As previously reported, both levodopa and dopamine inhibit complex I activity in a dose‐dependent manner. In contrast, the two major metabolites of dopamine, homovanillic acid and 3, 4‐dihydroxyphenylacetic acid as well as 3‐O‐methyl‐dopa, had little or no effect on complex I activities. Bromocriptine, pergolide, trihexyphenidyl, molindone, and clozapine were all without significant inhibitory effects on mitochondrial function. Although vitamin C and deprenyl did not alter complex I activity, they did prevent the inhibitory effect of both levodopa and dopamine on complex I activity. This work indicates that among the different and usual antiparkinsonian agents, only levodopa and dopamine induced reductions in complex I activity. It also indicates that vitamin C and deprenyl are both effective in preventing the levodopa‐induced complex I inhibition. This latter finding provides further support to the use of antioxidants and monoamine oxidase inhibitors as therapeutic strategies in attempts to slow the progression of PD.
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DOI: 10.1002/mds.870100314
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1995-05">1995-05</date><biblScope unit="volume">10</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="312">312</biblScope><biblScope unit="page" to="317">317</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">1EC2FAA20B18F1A8C6E8E844C2D57AC1DE45FA9E</idno><idno type="DOI">10.1002/mds.870100314</idno><idno type="ArticleID">MDS870100314</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Anticholinergic</term><term>Antioxidant</term><term>Complex I</term><term>Dopamine agonist</term><term>Levodopa</term><term>Mitochondria</term><term>Neuroleptic</term><term>Parkinson's disease</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Alterations in complex I activity, one of the enzymatic units of the mitochondrial respiratory chain, have been demonstrated in different tissues from patients with Parkinson's disease (PD). Subsequently, we showed that the chronic administration of levodopa can cause alterations in mitochondrial respiratory chain activity in rats, which suggests that the observed deficit in complex I activity in PD might be, at least in part, related to chronic levodopa therapy. Our study assessed the in vitro effects of different antiparkinsonian agents on complex I activity in rat brain. As previously reported, both levodopa and dopamine inhibit complex I activity in a dose‐dependent manner. In contrast, the two major metabolites of dopamine, homovanillic acid and 3, 4‐dihydroxyphenylacetic acid as well as 3‐O‐methyl‐dopa, had little or no effect on complex I activities. Bromocriptine, pergolide, trihexyphenidyl, molindone, and clozapine were all without significant inhibitory effects on mitochondrial function. Although vitamin C and deprenyl did not alter complex I activity, they did prevent the inhibitory effect of both levodopa and dopamine on complex I activity. This work indicates that among the different and usual antiparkinsonian agents, only levodopa and dopamine induced reductions in complex I activity. It also indicates that vitamin C and deprenyl are both effective in preventing the levodopa‐induced complex I inhibition. This latter finding provides further support to the use of antioxidants and monoamine oxidase inhibitors as therapeutic strategies in attempts to slow the progression of PD.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region><settlement><li>New York</li></settlement><orgName><li>Université Columbia</li></orgName></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Przedborski" sort="Przedborski" uniqKey="Przedborski" last="Przedborski">Przedborski</name></region><name sortKey="Fahn, Stanley" sort="Fahn, Stanley" uniqKey="Fahn S" first="Stanley" last="Fahn">Stanley Fahn</name><name sortKey="Jackson Ewis, Vernice" sort="Jackson Ewis, Vernice" uniqKey="Jackson Ewis V" first="Vernice" last="Jackson-Lewis">Vernice Jackson-Lewis</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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