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• W2043968213 abstract "Tao Xie and colleagues (June 21, p 1966)1Xie T Ho SL Ramsden D Catechol-O-methyltransferase inhibitors in Parkinson's disease.Lancet. 1998; 351: 1966Summary Full Text Full Text PDF PubMed Scopus (7) Google Scholar postulate a direct antidepressant effect of central catechol-O-methyltransferase inhibitors (COMT-I), such as tolcapone, because of an increased concentration of norepinephrine and S-adenosy1-Lmethionine (SAM) in the brain. Despite acute beneficial effects of central COMT-I on motor disability and depression, chronic treatment might induce neurotoxicity by blocking the physiological role of COMT. Physiologically, it eliminates biologically active toxic catechols and other hydrolated metabolites with potential endogenous or exogenous toxicity.COMT catalyses O-methylation of levodopa and dopamine to 3-Omethyldopa and 3-O-methyldopamine with SAM as methyldonor. There is experimental evidence that administration of tolcapone produces important COMT inhibition in the central nervous system with a concomitant dose-dependent increase of SAM in rat striatum.2Da Prada M Borgulya J Napolitano A et al.Improved therapy of Parkinson's disease with Tolcapone, a central and peripheral COMT Inhibitor with an S-Adenosyl-L-Methioninesparing effect.Clin Neuropharmacol. 1994; 17: S26-S37Crossref Google ScholarHowever, intracerebroventricular injection of SAM in rats causes symptoms similar to those of Parkinson's disease, which are caused by substantia nigra degeneration and tyrosine hydroxylase depletion.3Charlton CG Mack J Substantia nigra degeneration and tyrosine hydroxylase depletion caused by excess S-adenosylmethionine in the rat brain.Mol Neurobiol. 1994; 9: 149-161Crossref PubMed Scopus (29) Google Scholar Although the mechanism of this toxic process is unclear, central COMT-I might accelerate nigrostriatal degeneration in Parkinson's disease by a SAM-dependent increase of, for example, N-methylatian reactions.Tolcapone significantly increases 3,4-dihydroxyphenylacetic acid and lowers homovanillic acid and 3-methoxytyramine in the whole brain of the rat.4Zürcher G Dingemanse J Da Prada M Ro 40–7592, a potent inhibitor of extracerebral and brain Catechol-O-methyltransferase: preclinical and clinical findings.in: Agnoli A Campanella G New developments in therapy of Parkinson's disease. John Libbey, Rome1991: 37-43Google Scholar This effect is caused by reduced conversion of 3,4-dihydroxyphenylacetic acid to homovanillic acid by COMT and indicates enhanced oxidative desamination of dopamine via the monoaminooxidase (MAO)-metabolising pathway. Thus, increase of oxidative stress may be expected in neuronal and glial cells because of generation of H2O2 and neurocytotoxic hydroxyl radicals via MAO-A or MAO-B or both. Miller and colleagues5Miller JW Selhub J Joseph JA Oxidative damage caused by free radicals produced during catecholamine autoxidation: protective effects of O-methylation and melatonin.Free Radic Biol Med. 1996; 21: 241-249Crossref PubMed Scopus (138) Google Scholar have shown in an in-vitro model of catecholamine auto-oxidation that replacement of dopamine and levodopa by their O-methylated metabolites 3-OMD and 3-OMDA significantly decreases the rate of oxidation.5Miller JW Selhub J Joseph JA Oxidative damage caused by free radicals produced during catecholamine autoxidation: protective effects of O-methylation and melatonin.Free Radic Biol Med. 1996; 21: 241-249Crossref PubMed Scopus (138) Google Scholar Thus, O-methylation might be of physiological importance in the brain's antioxidant defence against catecholamine auto-oxidation.Central COMT-inhibition could induce neurotoxicity in patients with Parkinson's disease. However, experimental and clinical data on longterm effects are lacking. Tao Xie and colleagues (June 21, p 1966)1Xie T Ho SL Ramsden D Catechol-O-methyltransferase inhibitors in Parkinson's disease.Lancet. 1998; 351: 1966Summary Full Text Full Text PDF PubMed Scopus (7) Google Scholar postulate a direct antidepressant effect of central catechol-O-methyltransferase inhibitors (COMT-I), such as tolcapone, because of an increased concentration of norepinephrine and S-adenosy1-Lmethionine (SAM) in the brain. Despite acute beneficial effects of central COMT-I on motor disability and depression, chronic treatment might induce neurotoxicity by blocking the physiological role of COMT. Physiologically, it eliminates biologically active toxic catechols and other hydrolated metabolites with potential endogenous or exogenous toxicity. COMT catalyses O-methylation of levodopa and dopamine to 3-Omethyldopa and 3-O-methyldopamine with SAM as methyldonor. There is experimental evidence that administration of tolcapone produces important COMT inhibition in the central nervous system with a concomitant dose-dependent increase of SAM in rat striatum.2Da Prada M Borgulya J Napolitano A et al.Improved therapy of Parkinson's disease with Tolcapone, a central and peripheral COMT Inhibitor with an S-Adenosyl-L-Methioninesparing effect.Clin Neuropharmacol. 1994; 17: S26-S37Crossref Google Scholar However, intracerebroventricular injection of SAM in rats causes symptoms similar to those of Parkinson's disease, which are caused by substantia nigra degeneration and tyrosine hydroxylase depletion.3Charlton CG Mack J Substantia nigra degeneration and tyrosine hydroxylase depletion caused by excess S-adenosylmethionine in the rat brain.Mol Neurobiol. 1994; 9: 149-161Crossref PubMed Scopus (29) Google Scholar Although the mechanism of this toxic process is unclear, central COMT-I might accelerate nigrostriatal degeneration in Parkinson's disease by a SAM-dependent increase of, for example, N-methylatian reactions. Tolcapone significantly increases 3,4-dihydroxyphenylacetic acid and lowers homovanillic acid and 3-methoxytyramine in the whole brain of the rat.4Zürcher G Dingemanse J Da Prada M Ro 40–7592, a potent inhibitor of extracerebral and brain Catechol-O-methyltransferase: preclinical and clinical findings.in: Agnoli A Campanella G New developments in therapy of Parkinson's disease. John Libbey, Rome1991: 37-43Google Scholar This effect is caused by reduced conversion of 3,4-dihydroxyphenylacetic acid to homovanillic acid by COMT and indicates enhanced oxidative desamination of dopamine via the monoaminooxidase (MAO)-metabolising pathway. Thus, increase of oxidative stress may be expected in neuronal and glial cells because of generation of H2O2 and neurocytotoxic hydroxyl radicals via MAO-A or MAO-B or both. Miller and colleagues5Miller JW Selhub J Joseph JA Oxidative damage caused by free radicals produced during catecholamine autoxidation: protective effects of O-methylation and melatonin.Free Radic Biol Med. 1996; 21: 241-249Crossref PubMed Scopus (138) Google Scholar have shown in an in-vitro model of catecholamine auto-oxidation that replacement of dopamine and levodopa by their O-methylated metabolites 3-OMD and 3-OMDA significantly decreases the rate of oxidation.5Miller JW Selhub J Joseph JA Oxidative damage caused by free radicals produced during catecholamine autoxidation: protective effects of O-methylation and melatonin.Free Radic Biol Med. 1996; 21: 241-249Crossref PubMed Scopus (138) Google Scholar Thus, O-methylation might be of physiological importance in the brain's antioxidant defence against catecholamine auto-oxidation. Central COMT-inhibition could induce neurotoxicity in patients with Parkinson's disease. 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• W2043968213 title "Tolcapone and neurotoxicity in Parkinson's disease" @default.
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