Xenobiotic metabolism in Parkinson's disease

Neurology. 1989 Jul;39(7):883-7. doi: 10.1212/wnl.39.7.883.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetaminophen / metabolism
  • Humans
  • Parkinson Disease / metabolism*
  • Reference Values
  • Sulfates / metabolism
  • Sulfoxides / biosynthesis
  • Xenobiotics / metabolism


  • Sulfates
  • Sulfoxides
  • Xenobiotics
  • Acetaminophen