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Neurotoxicity of levodopa on catecholamine‐rich neurons

Neurotoxicity of levodopa on catecholamine‐rich neurons 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, (3H)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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Movement Disorders Wiley

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References (40)

Publisher
Wiley
Copyright
Copyright © 1992 Movement Disorder Society
ISSN
0885-3185
eISSN
1531-8257
DOI
10.1002/mds.870070105
pmid
1557063
Publisher site
See Article on Publisher Site

Abstract

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, (3H)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.

Journal

Movement DisordersWiley

Published: Jan 1, 1992

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