Xenobiotic metabolism in Parkinson's disease

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Abstract
We studied 68 patients with Parkinson9s 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.

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