Mitochondria-targeted antioxidant effects of S(-) and R(+) pramipexole.

Giulia Ferrari-Toninelli, Giuseppina Maccarinelli, Daniela Uberti, Erich Buerger, Maurizio Memo

Journal: BMC pharmacology 2010;10():2

PMID: 20137065

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Abstract

BACKGROUND

Pramipexole exists as two isomers. The S(-) enantiomer is a potent D3/D2 receptor agonist and is extensively used in the management of PD. In contrast, the R(+) enantiomer is virtually devoid of any of the DA agonist effects. Very limited studies are available to characterize the pharmacological spectrum of the R(+) enantiomer of pramipexole.

RESULTS

Using differentiated SH-SY5Y neuroblastoma cells as an experimental model, here we show that S(-) and R(+) pramipexole are endowed with equipotent efficacy in preventing cell death induced by H2O2 and inhibiting mitochondrial reactive oxygen species generation. Both pramipexole enantiomers prevented mitochondrial ROS generation with a potency about ten times higher then that elicited for neuroprotection.

CONCLUSIONS

These results support the concept of both S(-) and R(+) pramipexole enantiomers as mitochondria-targeted antioxidants and suggest that the antioxidant, neuroprotective activity of these drugs is independent of both the chiral 6-propylamino group in the pramipexole molecule and the DA receptor stimulation.

Address: Department of Biomedical Sciences and Biotechnologies and National Institute of Neuroscience, University of Brescia, Brescia, Italy.

DOI: 10.1186/1471-2210-10-2

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MeSH Terms: Antioxidants, Apoptosis, Benzothiazoles, Cell Culture Techniques, Cell Survival, Dopamine Antagonists, Drug Delivery Systems, Humans, Hydrogen Peroxide, Mitochondria, Neurons, Neuroprotective Agents, Oxidative Stress, Pramipexole, Reactive Oxygen Species, Rosiglitazone, Thiazolidinediones, Tumor Cells, Cultured