@article {Asanuma:July 2005:0161-6412:533,
	author = "Asanuma, Masato",
	author = "Miyazaki, Ikuko",
	author = "Diaz-Corrales, Francisco J.",
	author = "Shimizu, Masako",
	author = "Tanaka, Ken-ichi",
	author = "Ogawa, Norio",
	title = "Pramipexole has ameliorating effects on levodopa-induced abnormal dopamine turnover in parkinsonian striatum and quenching effects on dopamine-semiquinone generated in vitro",
	journal = "Neurological Research",
	volume = "27",
	year = "July 2005",
	abstract = "<B>Objectives and methods:</B> To clarify the effects of a non-ergot dopamine agonist pramipexole on levodopa-induced abnormal dopamine metabolism in the parkinsonian model, we examined striatal changes in dopamine and its metabolites after repeated administration of pramipexole and/or levodopa using 6-hydroxydopamine-lesioned hemi-parkinsonian mice. Moreover, the effects of pramipexole on dopamine-semiquinones were also accessed using an <I>in vitro</I> dopamine-semiquinone generating system to elucidate its neuroprotective property against dopamine quinone-induced neurotoxicity that appears as dopamine neuron-specific oxidative stress.<P></P><B>Results:</B> Combined administration of pramipexole (0.5 or 1 mg/kg/day, 7 days) selectively suppressed the levodopa-induced (50 mg/kg/day) increase of striatal dopamine turnover in the parkinsonian side, but not in the non-lesioned side. In addition to the antioxidant properties previously reported, it was clarified that pramipexole scavenged dopamine-semiquinones generated in a dose-dependent manner either in simultaneous incubation or post-incubation.<P></P><B>Discussion:</B> The neurotoxicity of dopamine quinones that appear as dopaminergic neuron-specific oxidative stress has recently been known to play a role in the pathogenesis of Parkinson's disease and neurotoxin-induced parkinsonism. Therefore, the present results revealed that pramipexole possesses neuroprotective effects against abnormal dopamine metabolism in excessively levodopa-administered parkinsonian brains and against cytotoxic dopamine quinones generated from excess dopamine, preventing consequently dopaminergic neuronal damage induced by excess dopamine or levodopa.",
	pages = "533-539(7)",
	url = "http://www.ingentaconnect.com/content/maney/nres/2005/00000027/00000005/art00013"
	doi = "doi:10.1179/016164105X22093"
}