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Neurotoxicity of levodopa on catecholamine‐rich neurons
Author(s) -
Mena María Angeles,
Pardo Beatriz,
Casarejos María José,
Fahn Stanley,
de Yébenes Justo García
Publication year - 1992
Publication title -
movement disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.352
H-Index - 198
eISSN - 1531-8257
pISSN - 0885-3185
DOI - 10.1002/mds.870070105
Subject(s) - levodopa , neurotoxicity , dopamine , catecholamine , monoamine oxidase , chemistry , monoamine oxidase inhibitor , pharmacology , monoamine neurotransmitter , toxicity , biochemistry , endocrinology , medicine , biology , parkinson's disease , enzyme , serotonin , receptor , disease , organic chemistry
The human neuroblastoma cells NB69 are a catecholamine‐rich cell line with pharmacological properties similar to dopamine neurons. This cell line was used to study the neurotoxicity of levodopa on catecholamine neurons. Levodopa, at 50 × 10 −6 M or higher concentrations, produced a doseand time‐dependent reduction in the number of live cells, [ 3 H]thymidine uptake, levels of protein and DNA, and an enhancement of the quinone formation. This is a specific effect of levodopa since it did not happen in NB69 cells incubated with equimolar concentrations of leucine and tryptophan. Treatment with deprenyl, an inhibitor of monoamine oxidase type B, partially prevented levodopa neurotoxicity, suggesting that the mechanism of toxicity was, at least in part, related to an increase in the metabolism of dopamine catalyzed by monoamine oxidase.

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