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  • Title: [Clinical significance of oxidation and acetylation genetic polymorphism in patients with Parkinson's disease].
    Author: Milejski P, Orzechowska-Juzwenko K, Kamienowski J, Horoch E, Niewiński P, Hurkacz M, Rzemisławska Z.
    Journal: Neurol Neurochir Pol; 1999; 33(5):1015-24. PubMed ID: 10672554.
    Abstract:
    The relationship between genetically determined polymorphic oxidation and acetylation and susceptibility to some disease has aroused much interest. The aim of our study was to evaluate whether patients with Parkinson's disease differ from healthy persons in their ability to oxidize sparteine and acetylate sulfadimidine as model drugs. Oxidation and acetylation phenotypes were estimated in 50 patients with Parkinson's disease. The control group consisted of 160 healthy volunteers for comparison of oxidation phenotype and 60 healthy volunteers for comparison of acetylation phenotype. The phenotyping of oxidation revealed two distinct populations among 50 patients with Parkinson's disease: 47 persons (94%) were extensive metabolizers of sparteine and 3 persons (6%) were poor metabolizers. In 160 healthy persons, 146 persons (91.2%) were extensive metabolizers of sparteine and 14 persons (8.8%) were poor metabolizers. The difference between frequency distribution of PMs and EMs in healthy persons and in patients with Parkinson's disease was not statistically significant. The phenotyping of acetylation showed among 50 patients with Parkinson's disease 38 persons (76%) slow acetylators and 12 persons (24%) rapid acetylators. In 60 healthy volunteers the phenotype of slow acetylation was observed in 29 persons (48.3%) and rapid acetylation in 31 persons (51.7%). The prevalence of slow acetylators among patients with Parkinson's disease in comparison to healthy volunteers was statistically significant (chi 2 = 8.7677/p < 0.003). The results of our study may suggest that the slow acetylation phenotype is associated with increased risk of the development of Parkinson's disease.
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