Taurine / metal-stimulated oxidation
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Date: 02/27/05
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Date: 27 Feb 2005 11:59:48 -0800
Neurotox Res. 2000 Jan;2(1):1-15. Related Articles, Links
Taurine inhibition of metal-stimulated catecholamine oxidation.
Dawson R Jr, Baker D, Eppler B, Tang E, Shih D, Hern H, Hu M.
Department of Pharmacodynamics, College of Pharmacy, JHMHC Box 100487,
University of Florida, Gainesville, FL 32610, USA.
Taurine is an abundant amino acid found in mammalian tissues and it has
been suggested to have cytoprotective functions. The aim of the present
study was to determine if taurine had the potential to reduce oxidative
stress associated with metal-stimulated catecholamine oxidation.
Taurine and structural analogs of taurine were tested for their ability
to inhibit metal-stimulated quinone formation from dopamine or L-dopa.
Oxidative damage to proteins and lipids were also assessed in vitro and
the effects of taurine were determined. Taurine (20 mM) was found to
decrease significantly ferric iron (50-500 microM)- and manganese (10
microM)-stimulated L-dopa or dopamine oxidation. Taurine had no effect
on zinc-induced dopamine oxidation and slightly potentiated copper- and
NaIO(4)-stimulated quinone formation. Ferric iron-stimulated lipid
peroxidation was not affected by taurine (1-20 mM). Protein carbonyl
formation induced by ferric iron (500 microM) and L-dopa (500 microM)
was significantly reduced by 10 mM taurine. The cytotoxicity of L-dopa
(250 microM) and ferric chloride (75 microM) to LLC-PK(1) cells was
attenuated by 10 mM taurine or hypotaurine. Homotaurine alone
stimulated L-dopa oxidation and potentiated the cytotoxic effects of
ferric iron. Homotaurine was found to be cytotoxic when combined with
L-dopa or L-dopa/iron. In contrast, hypotaurine inhibited quinone
formation and protected LLC-PK(1) cells. These studies suggest that
taurine may exhibit cytoprotective effects against the oxidation
products of catecholamines by acting as a scavenger for free radicals
and cytotoxic quinones.
PMID: 15545001 [PubMed - in process]
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