Linked Life Data

2788714

Source:http://linkedlifedata.com/resource/pubmed/id/2788714

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1989-10-12
pubmed:abstractText
The in vitro development of monoamine oxidase (MAO) activity and [3H]dopamine (DA) uptake capacity of dissociated cell cultures from rat embryo mesencephalon were correlated with the potency of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridine (MPP+) neurotoxicity. Specific activities of both MAO-A and MAO-B increased during in vitro development of the cultures, with MAO-B activity increasing 20-fold between the first and fourth week. Similarly, [3H]DA accumulation increased 2.6-fold between the first and third week in vitro, when it reached a plateau. Unexpectedly, the toxicities of MPTP and MPP+ were substantially decreased in the older cultures. Exposure to MPTP reduced [3H]DA accumulation per culture by 77% in 1-week-old cultures and by 36% in 4-week-old cultures. Similarly, damage caused by MPPT was reduced from 84% of control in the first week to 34% of control in the fourth week. The attenuation of neurotoxicity was not due to an increase in storage of MPP+ in the synaptic vesicles of DA neurons, nor to a change in the distribution of MPP+ between dopaminergic and other cellular components of the cultures. The damage to DA neurons caused by the mitochondrial toxin, rotenone, also showed a similar reduction in the older cultures. These observations coupled with an increase in lactate formation and glucose consumption during the in vitro development of the cultures suggest a shift toward increased glycolysis and decreased dependence on aerobic metabolism. This would render the cells more resistant to the inhibition of mitochondrial function by MPP+.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1149-55
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:2788714-1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, pubmed-meshheading:2788714-1-Methyl-4-phenylpyridinium, pubmed-meshheading:2788714-Animals, pubmed-meshheading:2788714-Cells, Cultured, pubmed-meshheading:2788714-Designer Drugs, pubmed-meshheading:2788714-Dopamine, pubmed-meshheading:2788714-Embryo, Mammalian, pubmed-meshheading:2788714-Isoenzymes, pubmed-meshheading:2788714-Kinetics, pubmed-meshheading:2788714-Mazindol, pubmed-meshheading:2788714-Mesencephalon, pubmed-meshheading:2788714-Monoamine Oxidase, pubmed-meshheading:2788714-Neurons, pubmed-meshheading:2788714-Neurotoxins, pubmed-meshheading:2788714-Pyridines, pubmed-meshheading:2788714-Pyridinium Compounds, pubmed-meshheading:2788714-Rats, pubmed-meshheading:2788714-Rats, Inbred Strains, pubmed-meshheading:2788714-Reserpine, pubmed-meshheading:2788714-Rotenone, pubmed-meshheading:2788714-Time Factors
pubmed:year
1989
pubmed:articleTitle
Mesencephalic dopamine neurons become less sensitive to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine toxicity during development in vitro.
pubmed:affiliation
Department of Neurology, Mount Sinai School of Medicine, New York, New York 10029.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't