Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1998-3-3
pubmed:abstractText
Recently, an endogenous catechol isoquinoline, 1(R),2(N)-dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline [N-methyl(R)salsolinol], was proved to be a neurotoxin specific for dopamine neurons by in vivo and in vitro experiments. This N-methyl(R)salsolinol was found to increase significantly in the cerebrospinal fluid of untreated parkinsonian patients, suggesting its possible involvement in the pathogenesis of Parkinson's disease. To clarify the mechanism of the increase, the activity of enzymes related to the metabolism of the neurotoxin was examined in lymphocytes prepared from parkinsonian patients and controls. In patients with Parkinson's disease, the activity of a neutral N-methyltransferase, measured by using (R)salsolinol as a substrate, was found to increase significantly (100.2 +/- 81.8 pmol/min/mg of protein) in comparison with that in controls (18.9 +/- 15.0 pmol/min/mg of protein). The distribution of the activity was bimodal in the parkinsonian patients, whereas it was singular in controls. The activity of other related enzymes, an alkaline N-methyltransferase and N-methyl(R)salsolinol oxidase, in parkinsonian lymphocytes was the same as in controls. Increase of the neutral N-methyltransferase may be an endogenous factor in the pathogenesis of Parkinson's disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0364-5134
pubmed:author
pubmed:issnType
Print
pubmed:volume
43
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
212-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
(R)salsolinol N-methyltransferase activity increases in parkinsonian lymphocytes.
pubmed:affiliation
Department of Biosciences, Nagoya Institute of Technology, Japan.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't