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Xenobiotic metabolism in Parkinson's disease

Department of Neurology, Queen Elizabeth Medical Centre, and Department of Biochemistry, University of Birmingham, United Kingdom

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 >,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.

Address correspondence and reprint requests to Dr. Williams, Department of Neurology, Queen Elizabeth Hospital, Queen Elizabeth Medical Centre, Edgbaston, Birmingham B15 2TH. UK.

Supported by both the Parkinson's Disease Society and the Motor Neurone Disease Association.

Received September 2, 1988. Accepted for publication in final form March 27,1989.

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