Metabolic stress in PC12 cells induces the formation of the endogenous dopaminergic neurotoxin, 3,4‐dihydroxyphenylacetaldehyde
Identifieur interne : 001C05 ( Main/Exploration ); précédent : 001C04; suivant : 001C06Metabolic stress in PC12 cells induces the formation of the endogenous dopaminergic neurotoxin, 3,4‐dihydroxyphenylacetaldehyde
Auteurs : I. Lamensdorf [États-Unis] ; G. Eisenhofer [États-Unis] ; J. Harvey-White [États-Unis] ; Y. Hayakawa [États-Unis] ; K. Kirk [États-Unis] ; I. J. Kopin [États-Unis]Source :
- Journal of Neuroscience Research [ 0360-4012 ] ; 2000-05-15.
English descriptors
Abstract
3,4‐Dihydroxyphenylacetaldehyde (DOPAL) has been reported to be a toxic metabolite formed by the oxidative‐deamination of dopamine (DA) catalyzed by monoamine oxidase. This aldehyde is either oxidized to 3,4‐dihydroxyphenylacetic acid (DOPAC) by aldehyde dehydrogenase, an NAD‐dependent enzyme or reduced to 3,4‐dihydroxyphenylethanol (DOPET) by aldehyde or aldose reductase. In the present study we examined whether levels of DOPAL are elevated by inhibition of the mitochondrial respiratory chain. Using inhibitors of mitochondrial complexes I, II, III and IV we found that inhibition of complex I and III increased levels of DOPAL and DOPET. Nerve growth factor‐induced differentiation of PC12 cells markedly potentiated DOPAL and DOPET accumulation in response to metabolic stress. DOPAL was toxic to differentiated PC12 as well as to SK‐N‐SH cell lines. Because complex I dysfunction has been implicated in the pathogenesis of Parkinson's disease, the accumulation of DOPAL may explain the vulnerability of the dopaminergic system to complex I inhibition. The rapid appearance of DOPAL and DOPET after inhibition of complex I may be a useful early index of oxidative stress in DA‐forming neurons. J. Neurosci. Res. 60:552–558, 2000 © 2000 Wiley‐Liss, Inc.
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DOI: 10.1002/(SICI)1097-4547(20000515)60:4<552::AID-JNR14>3.0.CO;2-U
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J." last="Kopin">I. J. Kopin</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:E4534647C2BAE4DA1A6E7DD27C128AD50F73D36F</idno><date when="2000" year="2000">2000</date><idno type="doi">10.1002/(SICI)1097-4547(20000515)60:4<552::AID-JNR14>3.0.CO;2-U</idno><idno type="url">https://api.istex.fr/document/E4534647C2BAE4DA1A6E7DD27C128AD50F73D36F/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001532</idno><idno type="wicri:Area/Main/Curation">001307</idno><idno type="wicri:Area/Main/Exploration">001C05</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Metabolic stress in PC12 cells induces the formation of the endogenous dopaminergic neurotoxin, 3,4‐dihydroxyphenylacetaldehyde</title><author><name sortKey="Lamensdorf, I" sort="Lamensdorf, I" uniqKey="Lamensdorf I" first="I." last="Lamensdorf">I. 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Res.</title><idno type="ISSN">0360-4012</idno><idno type="eISSN">1097-4547</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2000-05-15">2000-05-15</date><biblScope unit="volume">60</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="552">552</biblScope><biblScope unit="page" to="558">558</biblScope></imprint><idno type="ISSN">0360-4012</idno></series><idno type="istex">E4534647C2BAE4DA1A6E7DD27C128AD50F73D36F</idno><idno type="DOI">10.1002/(SICI)1097-4547(20000515)60:4<552::AID-JNR14>3.0.CO;2-U</idno><idno type="ArticleID">JNR14</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0360-4012</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>3,4‐dihydroxyphenylethanol</term><term>DOPAL</term><term>Parkinson's disease</term><term>complex I</term><term>dopamine</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">3,4‐Dihydroxyphenylacetaldehyde (DOPAL) has been reported to be a toxic metabolite formed by the oxidative‐deamination of dopamine (DA) catalyzed by monoamine oxidase. This aldehyde is either oxidized to 3,4‐dihydroxyphenylacetic acid (DOPAC) by aldehyde dehydrogenase, an NAD‐dependent enzyme or reduced to 3,4‐dihydroxyphenylethanol (DOPET) by aldehyde or aldose reductase. In the present study we examined whether levels of DOPAL are elevated by inhibition of the mitochondrial respiratory chain. Using inhibitors of mitochondrial complexes I, II, III and IV we found that inhibition of complex I and III increased levels of DOPAL and DOPET. Nerve growth factor‐induced differentiation of PC12 cells markedly potentiated DOPAL and DOPET accumulation in response to metabolic stress. DOPAL was toxic to differentiated PC12 as well as to SK‐N‐SH cell lines. Because complex I dysfunction has been implicated in the pathogenesis of Parkinson's disease, the accumulation of DOPAL may explain the vulnerability of the dopaminergic system to complex I inhibition. The rapid appearance of DOPAL and DOPET after inhibition of complex I may be a useful early index of oxidative stress in DA‐forming neurons. J. Neurosci. Res. 60:552–558, 2000 © 2000 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><country name="États-Unis"><region name="Maryland"><name sortKey="Lamensdorf, I" sort="Lamensdorf, I" uniqKey="Lamensdorf I" first="I." last="Lamensdorf">I. Lamensdorf</name></region><name sortKey="Eisenhofer, G" sort="Eisenhofer, G" uniqKey="Eisenhofer G" first="G." last="Eisenhofer">G. Eisenhofer</name><name sortKey="Harvey Hite, J" sort="Harvey Hite, J" uniqKey="Harvey Hite J" first="J." last="Harvey-White">J. Harvey-White</name><name sortKey="Hayakawa, Y" sort="Hayakawa, Y" uniqKey="Hayakawa Y" first="Y." last="Hayakawa">Y. Hayakawa</name><name sortKey="Kirk, K" sort="Kirk, K" uniqKey="Kirk K" first="K." last="Kirk">K. Kirk</name><name sortKey="Kopin, I J" sort="Kopin, I J" uniqKey="Kopin I" first="I. J." last="Kopin">I. J. Kopin</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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