ParkinsonFranceV1, PascalFrancis, Checkpoint, bibRecord, 000C52

Dopamine-derived salsolinol derivatives as endogenous monoamine oxidase inhibitors: Occurrence, metabolism and function in human brains

Identifieur interne : 000C52 ( PascalFrancis/Checkpoint ); précédent : 000C51; suivant : 000C53

Dopamine-derived salsolinol derivatives as endogenous monoamine oxidase inhibitors: Occurrence, metabolism and function in human brains

Auteurs : Makoto Naoi [Japon] ; Wakako Maruyama [Japon] ; Georgy M. Nagy [Hongrie]

Source :

Neurotoxicology : (Park Forest South) [ 0161-813X ] ; 2004.

RBID : Pascal:04-0191570

Descripteurs français

Pascal (Inist)
- Dopamine, Catécholamine, Stimulant dopaminergique, Salsolinol, Endogène, Oxidase, Inhibiteur, Métabolisme, Homme, Cerveau, Encéphale, Neurologie, Toxicologie.
Wicri :
- topic : Homme, Neurologie, Toxicologie.

English descriptors

KwdEn :
- Brain, Catecholamine, Dopamine, Dopamine agonist, Encephalon, Endogenous, Human, Inhibitor, Metabolism, Neurology, Oxidase, Toxicology.

Abstract

Salsolinol, 1-methyl-6, 7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, is an endogenous catechol isoquinoline detected in humans by M. Sandler. In human brain, a series of catechol isoquinolines were identified as the condensation products of dopamine or other monoamines with aldehydes or keto-acids. Recently selective occurrence of the (R)enantiomers of salsolinol derivatives was confirmed in human brain, and they are synthesized by enzymes in situ, but not by the non-enzymatic Pictet-Spengler reaction. A (R)salsolinol synthase catalyzes the enantio-specific synthesis of (R)salsolinol from dopamine and acetaldehyde, and (R)salsolinol N-methyltransferase synthesizes N-methyl(R)salsolinol, which is further oxidized into 1,2-dimethyl-6, 7-dihydroxyisoquinolinium ion by non-enzymatic and enzymatic oxidation. The stepwise reactions, N-methylation and oxidation, induce the specified distribution of the N-methylated and oxidized derivatives in the human nigro-striatum, suggesting that these derivatives may be involved in the function of dopamine neurons under physiological and pathological conditions. As shown by in vivo and in vitro experiments, salsolinol derivatives affect the levels of monoamine neurotransmitters though the inhibition of enzymes related in the metabolism of catechol- and indoleamines. In addition, the selective neurotoxicity of N-methyl(R)salsolinol to dopamine neurons was confirmed by preparation of an animal model of Parkinson's disease in rats. The involvement of N-methyl(R)salsolinol in the pathogenesis of Parkinson's disease was further indicated by the increase in the N-methyl(R)salsolinol levels in the cerebrospinal fluid and that in the activity of its synthesizing enzyme, a neural (R)salsolinol N-methyltransferase, in the lymphocytes prepared from parkinsonian patients. N-Methyl(R)salsolinol induces apoptosis in dopamine neurons, which is mediated by death signal transduction in mitochondria. In addition, salsolinol was found to function as a signal transmitter for the prolactin release in the neuro-intermediate lobe of the brain. These results are discussed in relation to role of dopamine-derived endogenous salsolinol derivatives as the regulators of neurotransmission, dopaminergic neurotoxins and neuro-hormonal transmitters in the human brain.

Affiliations:

Links toward previous steps (curation, corpus...)

to stream PascalFrancis, to step Corpus: 000E46
to stream PascalFrancis, to step Curation: 000588

Links to Exploration step

Pascal:04-0191570

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Dopamine-derived salsolinol derivatives as endogenous monoamine oxidase inhibitors: Occurrence, metabolism and function in human brains</title>
<author><name sortKey="Naoi, Makoto" sort="Naoi, Makoto" uniqKey="Naoi M" first="Makoto" last="Naoi">Makoto Naoi</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park</s1>
<s2>Matake, Gifu 505-0116</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
<country>Japon</country>
<wicri:noRegion>Matake, Gifu 505-0116</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Maruyama, Wakako" sort="Maruyama, Wakako" uniqKey="Maruyama W" first="Wakako" last="Maruyama">Wakako Maruyama</name>
<affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Basic Gerontology, National Institute for Longevity Sciences</s1>
<s2>Obu, Aichi 474-8522</s2>
<s3>JPN</s3>
<sZ>2 aut.</sZ>
</inist:fA14>
<country>Japon</country>
<wicri:noRegion>Obu, Aichi 474-8522</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Nagy, Georgy M" sort="Nagy, Georgy M" uniqKey="Nagy G" first="Georgy M." last="Nagy">Georgy M. Nagy</name>
<affiliation wicri:level="3"><inist:fA14 i1="03"><s1>Neuroendocrine Research Laboratory, Department of Human Morphology and Developmental Biology, Semmelweis University</s1>
<s2>Budapest</s2>
<s3>HUN</s3>
<sZ>3 aut.</sZ>
</inist:fA14>
<country>Hongrie</country>
<placeName><settlement type="city">Budapest</settlement>
<region nuts="2">Hongrie centrale</region>
</placeName>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">04-0191570</idno>
<date when="2004">2004</date>
<idno type="stanalyst">PASCAL 04-0191570 INIST</idno>
<idno type="RBID">Pascal:04-0191570</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">000E46</idno>
<idno type="wicri:Area/PascalFrancis/Curation">000588</idno>
<idno type="wicri:Area/PascalFrancis/Checkpoint">000C52</idno>
<idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000C52</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Dopamine-derived salsolinol derivatives as endogenous monoamine oxidase inhibitors: Occurrence, metabolism and function in human brains</title>
<author><name sortKey="Naoi, Makoto" sort="Naoi, Makoto" uniqKey="Naoi M" first="Makoto" last="Naoi">Makoto Naoi</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park</s1>
<s2>Matake, Gifu 505-0116</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
<country>Japon</country>
<wicri:noRegion>Matake, Gifu 505-0116</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Maruyama, Wakako" sort="Maruyama, Wakako" uniqKey="Maruyama W" first="Wakako" last="Maruyama">Wakako Maruyama</name>
<affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Basic Gerontology, National Institute for Longevity Sciences</s1>
<s2>Obu, Aichi 474-8522</s2>
<s3>JPN</s3>
<sZ>2 aut.</sZ>
</inist:fA14>
<country>Japon</country>
<wicri:noRegion>Obu, Aichi 474-8522</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Nagy, Georgy M" sort="Nagy, Georgy M" uniqKey="Nagy G" first="Georgy M." last="Nagy">Georgy M. Nagy</name>
<affiliation wicri:level="3"><inist:fA14 i1="03"><s1>Neuroendocrine Research Laboratory, Department of Human Morphology and Developmental Biology, Semmelweis University</s1>
<s2>Budapest</s2>
<s3>HUN</s3>
<sZ>3 aut.</sZ>
</inist:fA14>
<country>Hongrie</country>
<placeName><settlement type="city">Budapest</settlement>
<region nuts="2">Hongrie centrale</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Neurotoxicology : (Park Forest South)</title>
<title level="j" type="abbreviated">Neurotoxicology : (Park Forest South)</title>
<idno type="ISSN">0161-813X</idno>
<imprint><date when="2004">2004</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Neurotoxicology : (Park Forest South)</title>
<title level="j" type="abbreviated">Neurotoxicology : (Park Forest South)</title>
<idno type="ISSN">0161-813X</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Brain</term>
<term>Catecholamine</term>
<term>Dopamine</term>
<term>Dopamine agonist</term>
<term>Encephalon</term>
<term>Endogenous</term>
<term>Human</term>
<term>Inhibitor</term>
<term>Metabolism</term>
<term>Neurology</term>
<term>Oxidase</term>
<term>Toxicology</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Dopamine</term>
<term>Catécholamine</term>
<term>Stimulant dopaminergique</term>
<term>Salsolinol</term>
<term>Endogène</term>
<term>Oxidase</term>
<term>Inhibiteur</term>
<term>Métabolisme</term>
<term>Homme</term>
<term>Cerveau</term>
<term>Encéphale</term>
<term>Neurologie</term>
<term>Toxicologie</term>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term>
<term>Neurologie</term>
<term>Toxicologie</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Salsolinol, 1-methyl-6, 7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, is an endogenous catechol isoquinoline detected in humans by M. Sandler. In human brain, a series of catechol isoquinolines were identified as the condensation products of dopamine or other monoamines with aldehydes or keto-acids. Recently selective occurrence of the (R)enantiomers of salsolinol derivatives was confirmed in human brain, and they are synthesized by enzymes in situ, but not by the non-enzymatic Pictet-Spengler reaction. A (R)salsolinol synthase catalyzes the enantio-specific synthesis of (R)salsolinol from dopamine and acetaldehyde, and (R)salsolinol N-methyltransferase synthesizes N-methyl(R)salsolinol, which is further oxidized into 1,2-dimethyl-6, 7-dihydroxyisoquinolinium ion by non-enzymatic and enzymatic oxidation. The stepwise reactions, N-methylation and oxidation, induce the specified distribution of the N-methylated and oxidized derivatives in the human nigro-striatum, suggesting that these derivatives may be involved in the function of dopamine neurons under physiological and pathological conditions. As shown by in vivo and in vitro experiments, salsolinol derivatives affect the levels of monoamine neurotransmitters though the inhibition of enzymes related in the metabolism of catechol- and indoleamines. In addition, the selective neurotoxicity of N-methyl(R)salsolinol to dopamine neurons was confirmed by preparation of an animal model of Parkinson's disease in rats. The involvement of N-methyl(R)salsolinol in the pathogenesis of Parkinson's disease was further indicated by the increase in the N-methyl(R)salsolinol levels in the cerebrospinal fluid and that in the activity of its synthesizing enzyme, a neural (R)salsolinol N-methyltransferase, in the lymphocytes prepared from parkinsonian patients. N-Methyl(R)salsolinol induces apoptosis in dopamine neurons, which is mediated by death signal transduction in mitochondria. In addition, salsolinol was found to function as a signal transmitter for the prolactin release in the neuro-intermediate lobe of the brain. These results are discussed in relation to role of dopamine-derived endogenous salsolinol derivatives as the regulators of neurotransmission, dopaminergic neurotoxins and neuro-hormonal transmitters in the human brain.</div>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0161-813X</s0>
</fA01>
<fA03 i2="1"><s0>Neurotoxicology : (Park Forest South)</s0>
</fA03>
<fA05><s2>25</s2>
</fA05>
<fA06><s2>1-2</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Dopamine-derived salsolinol derivatives as endogenous monoamine oxidase inhibitors: Occurrence, metabolism and function in human brains</s1>
</fA08>
<fA09 i1="01" i2="1" l="ENG"><s1>Monoamine Oxidases: Molecular, Pharmacological and Neurotoxicological Aspects. A Tribute to Prof. Merton Sandler</s1>
</fA09>
<fA11 i1="01" i2="1"><s1>NAOI (Makoto)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>MARUYAMA (Wakako)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>NAGY (Georgy M.)</s1>
</fA11>
<fA12 i1="01" i2="1"><s1>NICOTRA (A.)</s1>
<s9>ed.</s9>
</fA12>
<fA12 i1="02" i2="1"><s1>PARVEZ (S. H.)</s1>
<s9>ed.</s9>
</fA12>
<fA12 i1="03" i2="1"><s1>GLOVER (V.)</s1>
<s9>ed.</s9>
</fA12>
<fA12 i1="04" i2="1"><s1>SANDLER (M.)</s1>
<s9>ed.</s9>
</fA12>
<fA12 i1="05" i2="1"><s1>PARVEZ (S.)</s1>
<s9>ed.</s9>
</fA12>
<fA12 i1="06" i2="1"><s1>MINAMI (M.)</s1>
<s9>ed.</s9>
</fA12>
<fA14 i1="01"><s1>Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park</s1>
<s2>Matake, Gifu 505-0116</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Department of Basic Gerontology, National Institute for Longevity Sciences</s1>
<s2>Obu, Aichi 474-8522</s2>
<s3>JPN</s3>
<sZ>2 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Neuroendocrine Research Laboratory, Department of Human Morphology and Developmental Biology, Semmelweis University</s1>
<s2>Budapest</s2>
<s3>HUN</s3>
<sZ>3 aut.</sZ>
</fA14>
<fA15 i1="01"><s1>Dept. Animal and Human Biology, University of Rome I, Viale dell'Università 32</s1>
<s2>00198 Rome</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
</fA15>
<fA15 i1="02"><s1>Institut Alfred Fressard of Neuroscience, Bât5 Parc Chateau, CNRS</s1>
<s2>91190 Gif sur Yvette</s2>
<s3>FRA</s3>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
</fA15>
<fA15 i1="03"><s1>Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, Du Cane Road</s1>
<s2>London, W12 ONN</s2>
<s3>GBR</s3>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</fA15>
<fA15 i1="04"><s1>The Research Institute of Personalized Health, Health Sciences University of Hokkaido</s1>
<s2>061-0293 Ishikari-Tobetsu</s2>
<s3>JPN</s3>
<sZ>6 aut.</sZ>
</fA15>
<fA20><s1>193-204</s1>
</fA20>
<fA21><s1>2004</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>18397</s2>
<s5>354000119285470200</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2004 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>2 p.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>04-0191570</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Neurotoxicology : (Park Forest South)</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Salsolinol, 1-methyl-6, 7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, is an endogenous catechol isoquinoline detected in humans by M. Sandler. In human brain, a series of catechol isoquinolines were identified as the condensation products of dopamine or other monoamines with aldehydes or keto-acids. Recently selective occurrence of the (R)enantiomers of salsolinol derivatives was confirmed in human brain, and they are synthesized by enzymes in situ, but not by the non-enzymatic Pictet-Spengler reaction. A (R)salsolinol synthase catalyzes the enantio-specific synthesis of (R)salsolinol from dopamine and acetaldehyde, and (R)salsolinol N-methyltransferase synthesizes N-methyl(R)salsolinol, which is further oxidized into 1,2-dimethyl-6, 7-dihydroxyisoquinolinium ion by non-enzymatic and enzymatic oxidation. The stepwise reactions, N-methylation and oxidation, induce the specified distribution of the N-methylated and oxidized derivatives in the human nigro-striatum, suggesting that these derivatives may be involved in the function of dopamine neurons under physiological and pathological conditions. As shown by in vivo and in vitro experiments, salsolinol derivatives affect the levels of monoamine neurotransmitters though the inhibition of enzymes related in the metabolism of catechol- and indoleamines. In addition, the selective neurotoxicity of N-methyl(R)salsolinol to dopamine neurons was confirmed by preparation of an animal model of Parkinson's disease in rats. The involvement of N-methyl(R)salsolinol in the pathogenesis of Parkinson's disease was further indicated by the increase in the N-methyl(R)salsolinol levels in the cerebrospinal fluid and that in the activity of its synthesizing enzyme, a neural (R)salsolinol N-methyltransferase, in the lymphocytes prepared from parkinsonian patients. N-Methyl(R)salsolinol induces apoptosis in dopamine neurons, which is mediated by death signal transduction in mitochondria. In addition, salsolinol was found to function as a signal transmitter for the prolactin release in the neuro-intermediate lobe of the brain. These results are discussed in relation to role of dopamine-derived endogenous salsolinol derivatives as the regulators of neurotransmission, dopaminergic neurotoxins and neuro-hormonal transmitters in the human brain.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A25</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B03</s0>
</fC02>
<fC02 i1="03" i2="X"><s0>002B17</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Dopamina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Catécholamine</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Catecholamine</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Catecolamina</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Stimulant dopaminergique</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Dopamine agonist</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Estimulante dopaminérgico</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Salsolinol</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Endogène</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Endogenous</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Endógeno</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Oxidase</s0>
<s2>FE</s2>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Oxidase</s0>
<s2>FE</s2>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Oxidase</s0>
<s2>FE</s2>
<s5>11</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Inhibiteur</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Inhibitor</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Inhibidor</s0>
<s5>12</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Métabolisme</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Metabolism</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Metabolismo</s0>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Homme</s0>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Human</s0>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Hombre</s0>
<s5>15</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Cerveau</s0>
<s5>16</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Brain</s0>
<s5>16</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Cerebro</s0>
<s5>16</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Encéphale</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Encephalon</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Encéfalo</s0>
<s5>17</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Neurologie</s0>
<s5>18</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Neurology</s0>
<s5>18</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Neurología</s0>
<s5>18</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Toxicologie</s0>
<s5>19</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Toxicology</s0>
<s5>19</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Toxicología</s0>
<s5>19</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fN21><s1>131</s1>
</fN21>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
<affiliations><list><country><li>Hongrie</li>
<li>Japon</li>
</country>
<region><li>Hongrie centrale</li>
</region>
<settlement><li>Budapest</li>
</settlement>
</list>
<tree><country name="Japon"><noRegion><name sortKey="Naoi, Makoto" sort="Naoi, Makoto" uniqKey="Naoi M" first="Makoto" last="Naoi">Makoto Naoi</name>
</noRegion>
<name sortKey="Maruyama, Wakako" sort="Maruyama, Wakako" uniqKey="Maruyama W" first="Wakako" last="Maruyama">Wakako Maruyama</name>
</country>
<country name="Hongrie"><region name="Hongrie centrale"><name sortKey="Nagy, Georgy M" sort="Nagy, Georgy M" uniqKey="Nagy G" first="Georgy M." last="Nagy">Georgy M. Nagy</name>
</region>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/PascalFrancis/Checkpoint

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000C52 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Checkpoint/biblio.hfd -nk 000C52 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Sante
   |area=    ParkinsonFranceV1
   |flux=    PascalFrancis
   |étape=   Checkpoint
   |type=    RBID
   |clé=     Pascal:04-0191570
   |texte=   Dopamine-derived salsolinol derivatives as endogenous monoamine oxidase inhibitors: Occurrence, metabolism and function in human brains
}}

This area was generated with Dilib version V0.6.29.
Data generation: Wed May 17 19:46:39 2017. Site generation: Mon Mar 4 15:48:15 2024

	La maladie de Parkinson en France (serveur d'exploration)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

La maladie de Parkinson en France (serveur d'exploration)

Dopamine-derived salsolinol derivatives as endogenous monoamine oxidase inhibitors: Occurrence, metabolism and function in human brains

Dopamine-derived salsolinol derivatives as endogenous monoamine oxidase inhibitors: Occurrence, metabolism and function in human brains

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri