Elevated activity of phospholipid biosynthetic enzymes in substantia nigra of patients with Parkinson's disease
Identifieur interne : 000B11 ( PascalFrancis/Checkpoint ); précédent : 000B10; suivant : 000B12Elevated activity of phospholipid biosynthetic enzymes in substantia nigra of patients with Parkinson's disease
Auteurs : B. M. Ross [Canada] ; N. Mamalias [Canada] ; A. Moszczynska [Canada] ; A. H. Rajput [Canada] ; S. J. Kish [Canada]Source :
- Neuroscience [ 0306-4522 ] ; 2001.
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- Pascal (Inist)
- Wicri :
- topic : Homme.
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Abstract
We reported that the activities of phospholipase A2, phosphocholine cytidylyltransferase and phosphoethanol-amine cytidylyltransferase, key phospholipid metabolic enzymes, are low in substantia nigra of normal human brain and that this might reduce the ability of nigral neurons to repair damage to cell membranes. To determine whether adaptive changes in nigral phospholipid metabolism can occur in idiopathic Parkinson's disease we compared activities of I 1 catabolic and anabolic enzymes in autopsied brain of 10 patients with Parkinson's disease to those in control subjects. Nigral activity of the catabolic enzyme phospholipase A2 was normal in the Parkinson's disease group, whereas that of the biosynthetic enzymes phosphoethanolamine cytidylyltransferase, phosphocholine cytidylyltransferase, and phosphatidylserine synthase were elevated 193, 48 and 38%, respectively, possibly representing a compensatory response to repair membrane phospholipids. Enzyme activities were normal in all other brain areas with the exception of increased (+26%) activity of calcium-stimulated phospholipase A2 in putamen, a change which could he consequent to either decreased dopaminergic striatal input or to a dopamine nerve terminal degenerative process. Our data indicate that the normally low rate of membrane phospholipid synthesis in the substantia nigra, the primary area of neurodegeneration in Parkinson's disease, is increased during the course of the disorder. We suggest that pharmacotherapies which augment this compensatory response might have utility as a treatment for Parkinson's disease.
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Ross</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Centre for Addiction and Mental Health, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Psychiatry, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation></author><author><name sortKey="Mamalias, N" sort="Mamalias, N" uniqKey="Mamalias N" first="N." last="Mamalias">N. 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M." last="Ross">B. M. Ross</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Centre for Addiction and Mental Health, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Psychiatry, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation></author><author><name sortKey="Mamalias, N" sort="Mamalias, N" uniqKey="Mamalias N" first="N." last="Mamalias">N. Mamalias</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Centre for Addiction and Mental Health, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation></author><author><name sortKey="Moszczynska, A" sort="Moszczynska, A" uniqKey="Moszczynska A" first="A." last="Moszczynska">A. Moszczynska</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Centre for Addiction and Mental Health, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation></author><author><name sortKey="Rajput, A H" sort="Rajput, A H" uniqKey="Rajput A" first="A. H." last="Rajput">A. H. Rajput</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Department of Neurology, University of Saskatchewan</s1><s2>Saskatoon, Saskatchewan</s2><s3>CAN</s3><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Saskatoon, Saskatchewan</wicri:noRegion></affiliation></author><author><name sortKey="Kish, S J" sort="Kish, S J" uniqKey="Kish S" first="S. J." last="Kish">S. J. Kish</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Centre for Addiction and Mental Health, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Psychiatry, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation></author></analytic><series><title level="j" type="main">Neuroscience</title><title level="j" type="abbreviated">Neuroscience</title><idno type="ISSN">0306-4522</idno><imprint><date when="2001">2001</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Neuroscience</title><title level="j" type="abbreviated">Neuroscience</title><idno type="ISSN">0306-4522</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Biosynthesis</term><term>Enzymatic activity</term><term>Human</term><term>Locus niger</term><term>Oxidative stress</term><term>Parkinson disease</term><term>Phospholipid</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Phospholipide</term><term>Biosynthèse</term><term>Activité enzymatique</term><term>Locus niger</term><term>Stress oxydatif</term><term>Parkinson maladie</term><term>Homme</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We reported that the activities of phospholipase A<sub>2</sub>, phosphocholine cytidylyltransferase and phosphoethanol-amine cytidylyltransferase, key phospholipid metabolic enzymes, are low in substantia nigra of normal human brain and that this might reduce the ability of nigral neurons to repair damage to cell membranes. To determine whether adaptive changes in nigral phospholipid metabolism can occur in idiopathic Parkinson's disease we compared activities of I 1 catabolic and anabolic enzymes in autopsied brain of 10 patients with Parkinson's disease to those in control subjects. Nigral activity of the catabolic enzyme phospholipase A<sub>2</sub> was normal in the Parkinson's disease group, whereas that of the biosynthetic enzymes phosphoethanolamine cytidylyltransferase, phosphocholine cytidylyltransferase, and phosphatidylserine synthase were elevated 193, 48 and 38%, respectively, possibly representing a compensatory response to repair membrane phospholipids. Enzyme activities were normal in all other brain areas with the exception of increased (+26%) activity of calcium-stimulated phospholipase A<sub>2</sub> in putamen, a change which could he consequent to either decreased dopaminergic striatal input or to a dopamine nerve terminal degenerative process. Our data indicate that the normally low rate of membrane phospholipid synthesis in the substantia nigra, the primary area of neurodegeneration in Parkinson's disease, is increased during the course of the disorder. We suggest that pharmacotherapies which augment this compensatory response might have utility as a treatment for Parkinson's disease.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0306-4522</s0></fA01><fA02 i1="01"><s0>NRSCDN</s0></fA02><fA03 i2="1"><s0>Neuroscience</s0></fA03><fA05><s2>102</s2></fA05><fA06><s2>4</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Elevated activity of phospholipid biosynthetic enzymes in substantia nigra of patients with Parkinson's disease</s1></fA08><fA11 i1="01" i2="1"><s1>ROSS (B. M.)</s1></fA11><fA11 i1="02" i2="1"><s1>MAMALIAS (N.)</s1></fA11><fA11 i1="03" i2="1"><s1>MOSZCZYNSKA (A.)</s1></fA11><fA11 i1="04" i2="1"><s1>RAJPUT (A. H.)</s1></fA11><fA11 i1="05" i2="1"><s1>KISH (S. J.)</s1></fA11><fA14 i1="01"><s1>Centre for Addiction and Mental Health, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Psychiatry, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="03"><s1>Department of Neurology, University of Saskatchewan</s1><s2>Saskatoon, Saskatchewan</s2><s3>CAN</s3><sZ>4 aut.</sZ></fA14><fA20><s1>899-904</s1></fA20><fA21><s1>2001</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>17194</s2><s5>354000097325620130</s5></fA43><fA44><s0>0000</s0><s1>© 2001 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>37 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>01-0144147</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Neuroscience</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>We reported that the activities of phospholipase A<sub>2</sub>, phosphocholine cytidylyltransferase and phosphoethanol-amine cytidylyltransferase, key phospholipid metabolic enzymes, are low in substantia nigra of normal human brain and that this might reduce the ability of nigral neurons to repair damage to cell membranes. To determine whether adaptive changes in nigral phospholipid metabolism can occur in idiopathic Parkinson's disease we compared activities of I 1 catabolic and anabolic enzymes in autopsied brain of 10 patients with Parkinson's disease to those in control subjects. Nigral activity of the catabolic enzyme phospholipase A<sub>2</sub> was normal in the Parkinson's disease group, whereas that of the biosynthetic enzymes phosphoethanolamine cytidylyltransferase, phosphocholine cytidylyltransferase, and phosphatidylserine synthase were elevated 193, 48 and 38%, respectively, possibly representing a compensatory response to repair membrane phospholipids. Enzyme activities were normal in all other brain areas with the exception of increased (+26%) activity of calcium-stimulated phospholipase A<sub>2</sub> in putamen, a change which could he consequent to either decreased dopaminergic striatal input or to a dopamine nerve terminal degenerative process. Our data indicate that the normally low rate of membrane phospholipid synthesis in the substantia nigra, the primary area of neurodegeneration in Parkinson's disease, is increased during the course of the disorder. We suggest that pharmacotherapies which augment this compensatory response might have utility as a treatment for Parkinson's disease.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17G</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Phospholipide</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Phospholipid</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Fosfolípido</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Biosynthèse</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Biosynthesis</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Biosíntesis</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Activité enzymatique</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Enzymatic activity</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Actividad enzimática</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Locus niger</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Locus niger</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Locus níger</s0><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Stress oxydatif</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Oxidative stress</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Stress oxidativo</s0><s5>05</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Parkinson maladie</s0><s5>09</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Parkinson disease</s0><s5>09</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s5>09</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Homme</s0><s5>54</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Human</s0><s5>54</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Hombre</s0><s5>54</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Encéphale</s0><s5>29</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Brain (vertebrata)</s0><s5>29</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo</s0><s5>29</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central</s0><s5>30</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system</s0><s5>30</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervioso central</s0><s5>30</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Système nerveux pathologie</s0><s5>38</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>38</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>38</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0><s5>39</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>39</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>39</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Encéphale pathologie</s0><s5>40</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>40</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>40</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0><s5>41</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>41</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>41</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>42</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>42</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>42</s5></fC07><fN21><s1>092</s1></fN21></pA></standard></inist><affiliations><list><country><li>Canada</li></country><region><li>Ontario</li></region><settlement><li>Toronto</li></settlement><orgName><li>Université de Toronto</li></orgName></list><tree><country name="Canada"><region name="Ontario"><name sortKey="Ross, B M" sort="Ross, B M" uniqKey="Ross B" first="B. M." last="Ross">B. M. Ross</name></region><name sortKey="Kish, S J" sort="Kish, S J" uniqKey="Kish S" first="S. J." last="Kish">S. J. Kish</name><name sortKey="Kish, S J" sort="Kish, S J" uniqKey="Kish S" first="S. J." last="Kish">S. J. Kish</name><name sortKey="Mamalias, N" sort="Mamalias, N" uniqKey="Mamalias N" first="N." last="Mamalias">N. Mamalias</name><name sortKey="Moszczynska, A" sort="Moszczynska, A" uniqKey="Moszczynska A" first="A." last="Moszczynska">A. Moszczynska</name><name sortKey="Rajput, A H" sort="Rajput, A H" uniqKey="Rajput A" first="A. H." last="Rajput">A. H. Rajput</name><name sortKey="Ross, B M" sort="Ross, B M" uniqKey="Ross B" first="B. M." last="Ross">B. M. Ross</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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