title: Xenobiotic metabolism in Parkinson's disease.
abstract: We studied 68 patients with Parkinson's disease (PD) with probe drugs to determine whether a defect in metabolism might be an etiologic factor and found no difference between patients and controls in their ability to form the 4-hydroxy metabolite of debrisoquin. However, using S-carboxymethyl-L-cysteine, 63.2% (43/68) of PD patients had reduced S-oxidation capacity, while 35.3% (24/68) produced no sulfoxides (controls, 35.2% and 2.5%). When we studied acetaminophen (paracetamol) metabolism, only 29.6% of PD patients excreted greater than 5% of the dose as the sulfate conjugate; the corresponding figure for controls was 83.9%. These results suggest a deficiency in detoxication pathways involving sulfur metabolism. PD patients may be unusually susceptible to exogenous or even endogenous toxins.
authors.affiliation: Department of Neurology, Queen Elizabeth Medical Centre, Birmingham, UK.
authors.forename: G B
authors.initials: GB
authors.lastname: Steventon
authors.forename: M T
authors.initials: MT
authors.lastname: Heafield
authors.forename: R H
authors.initials: RH
authors.lastname: Waring
authors.forename: A C
authors.initials: AC
authors.lastname: Williams
mesh_terms: D000082:Acetaminophen / Q000378:metabolism; D006801:Humans; D010300:Parkinson Disease / Q000378:metabolism*; D012016:Reference Values; D013431:Sulfates / Q000378:metabolism; D013454:Sulfoxides / Q000096:biosynthesis; D015262:Xenobiotics / Q000378:metabolism
chemical_list: D013431:Sulfates; D013454:Sulfoxides; D015262:Xenobiotics; D000082:Acetaminophen