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salsolinol/necrosis
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6 resultados
Differential cell death induced by salsolinol with and without copper: possible role of reactive oxygen species.
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Salsolinol (SAL), a novel dopaminergic catechol tetrahydroisoquinoline neurotoxin, has been speculated to contribute to the etiology of Parkinson's disease and neuropathology of chronic alcoholism. Our previous studies have demonstrated that SAL induces strand scission in øX174 supercoiled DNA and
Oxidation of N-methyl(R)salsolinol: involvement to neurotoxicity and neuroprotection by endogenous catechol isoquinolines.
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1(R), 2(N)-Dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, N-methyl(R)salsolinol, is a potent dopaminergic neurotoxin to induce parkinsonism in rats. The cytotoxicity of N-methyl(R)salsolinol proved to be ascribed to its oxidation into cytotoxic 1,2-dimethyl-6,7-dihydroxyisoquinolinium ion
Neurotoxins and neurotoxic species implicated in neurodegeneration.
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Neurotoxins, in the general sense, represent novel chemical structures which when administered in vivo or in vitro, are capable of producing neuronal damage or neurodegeneration--with some degree of specificity relating to neuronal phenotype or populations of neurons with specific characteristics
Cytotoxicity of dopamine-derived tetrahydroisoquinolines on melanoma cells.
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Tetrahydroisoquinolines (TIQs) are endogenous alkaloid compounds detected in urine, central nervous system and some peripheral tissues in Mammalia. No data are at present available on TIQ levels in skin, although in vitro biochemical evidences indicate that they may undergo auto-oxidation with
Research on an in vitro cell system for testing the neurotoxicity of kynurenine pathway metabolites.
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Quinolinic acid (QUIN), kynurenine acid (KYNA) and 3-hydroxykynurenine (3-HK) - metabolites of the kynurenine pathway are considered to be associated with many central nervous system diseases. However, in neuroscience research in order to test neurotoxicity or neuroprotection against these compounds
Neuroprotection by propargylamines in Parkinson's disease: suppression of apoptosis and induction of prosurvival genes.
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In Parkinson's disease (PD), therapies to delay or suppress the progression of cell death in nigrostriatal dopamine neurons have been proposed by use of various agents. An inhibitor of type B monoamine oxidase (MAO-B), (-)deprenyl (selegiline), was reported to have neuroprotective activity, but
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