MAO and L-dopa treatment of Parkinson's disease.
The aim of this study was to determine whether there were differences in the oxidative deamination of dopamine in patients with Parkinson's disease who demonstrated a long-duration response (LDR) to treatment with dopa and carbidopa and in patients who demonstrated only a short-duration response (SDR) to the drugs. The patients who demonstrated LDR had received dopa and carbidopa for a shorter time (3.4y) than had the SDR patients (9.5y). The concentrations of dopamine and 3-methoxytyramine and their deaminated metabolites 3,4-dihydroxyphenylacetic acid and homovanillic acid were measured in 24-h urine samples collected from patients in both groups. The ratios of homovanillic acid to 3-methoxytyramine and dopamine were greater in SDR than in LDR patients suggesting increased oxidative deamination of dopamine in this group. Increased oxidative deamination could be caused by an increase in MAO activity as Parkinson's disease progresses or by the treatment with L-dopa.
Tyce
G M
GM
Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota.
Dousa
M K
MK
Muenter
M D
MD
D000368:Aged; D002230:Carbidopa / Q000378:metabolism / Q000627:therapeutic use*; D004298:Dopamine / Q000652:urine*; D004338:Drug Combinations; D005260:Female; D006719:Homovanillic Acid / Q000652:urine; D006801:Humans; D007980:Levodopa / Q000378:metabolism / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D008995:Monoamine Oxidase / Q000378:metabolism*; D010300:Parkinson Disease / Q000188:drug therapy* / Q000201:enzymology / Q000652:urine
D004338:Drug Combinations; D007980:Levodopa; D008995:Monoamine Oxidase; D002230:Carbidopa; D004298:Dopamine; D006719:Homovanillic Acid