MAO and L-DOPA treatment of Parkinson’s disease

  • G. M. Tyce
  • M. K. Dousa
  • M. D. Muenter
Part of the Journal of Neural Transmission book series (NEURAL SUPPL, volume 29)


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 (3.4 y) than had the SDR patients (9.5 y). 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.


Tyrosine Hydroxylase Homovanillic Acid Mandelic Acid Oxidative Deamination Disodium EDTA 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. Birkmayer W, Riederer P, Ambrozi L, Youdim MBH (1977) Implications of combined treatment with “Madopar” and L-deprenil in Parkinson’s disease. Lancet i: 439–443.CrossRefGoogle Scholar
  2. Birkmayer W, Riederer P, Youdim MBH, Linauer W (1975) Potentiation of anti-akinetic effect after L-dopa treatment by an inhibitor of MAO-B, deprenil. J Neural Transm 36: 303–323.PubMedCrossRefGoogle Scholar
  3. Dairman W, Udenfriend S (1971) Decrease in adrenal tyrosine hydroxylase and increase in norepinephrine synthesis in rats given L-dopa. Science 171: 1022–1024.PubMedCrossRefGoogle Scholar
  4. Hoeldtke R, Rogawski M, Wurtman RJ (1974) Effect of selective destruction of central and peripheral catecholamine-containing neurones with 6-hydroxydopamine on cate-cholamine excretion in the rat. Br J Pharmacol 50: 265–270.PubMedGoogle Scholar
  5. Jellinger K, Riederer P (1984) Dementia in Parkinson’s disease and (pre)senile dementia of Alzheimer type. Morphological aspects and changes in the intracerebral MAO activity. Adv Neurol 40: 199–210.PubMedGoogle Scholar
  6. Knoll J (1986) Critical role of MAO inhibition in Parkinson’s disease. Adv Neurol 45: 107–110.Google Scholar
  7. Lewitt PA, Oxenkrug GF, McIntyre IM, McCauley RM (1985) Peripheral carbidopa effects monoamine oxidase. Neurology 35: 1258–1259.PubMedGoogle Scholar
  8. Molinoff PB, Brimijoin S, Axelrod J (1972) Induction of dopamine-β-hydroxylase and tyrosine hydroxylase in rat hearts and sympathetic ganglia. J Pharmacol Exp Ther 182: 116–129.PubMedGoogle Scholar
  9. Muenter MD, Tyce GM (1971) L-Dopa therapy of Parkinson’s disease: plasma L-dopa concentration, therapeutic response, and side effects. Mayo Clin Proc 46: 231–239.PubMedGoogle Scholar
  10. Muskiet FAJ, Fremouw-Ottevangers DC, van der Meulen J, Wolthers BG, de Vries JA (1978) Determination of some L-3,4-dihydroxyphenylalanine and dopamine metabolites in urine by means of mass fragmentography. Clin Chem 24: 122–127.PubMedGoogle Scholar
  11. Naoi M, Nagatsu T (1987) Inhibition of monoamine oxidase by 3,4-dihydroxyphenyl-L-alanine and its analogues. Life Sci 40: 321–328.PubMedCrossRefGoogle Scholar
  12. Sharpless NS, Tyce GM, Muenter MD, Dinapoli RP (1974) Dopa, 3-O-methyldopa, and metabolites in urine during oral L-3-O-methyldopa therapy. Clin Pharmacol Ther 16: 770–781.PubMedGoogle Scholar
  13. Sharpless NS, Tyce GM, Owen CA Jr (1973) Effect of chronic administration of L-dopa on catechol-O-methyltransferase in rat tissues. Life Sci 12: 97–106.CrossRefGoogle Scholar
  14. Spina MB, Cohen G (1989) Dopamine turnover and glutathione oxidation: implications for Parkinson’s disease. Proc Natl Acad Sci 86: 1398–1400.PubMedCrossRefGoogle Scholar
  15. Strolin-Benedetti MS, Dostert P (1989) Monoamine oxidase, brain ageing and degenerative diseases. Biochem Pharmacol 38: 555–561.PubMedCrossRefGoogle Scholar
  16. Tate SS, Sweet R, McDowell FH, Meister A (1971) Decrease of the 3,4-dihydroxyphen-ylalanine (DOPA) decarboxylase activities in human erythrocytes and mouse tissues after administration of DOPA. Proc Natl Acad Sci 68: 2121–2123.PubMedCrossRefGoogle Scholar
  17. Tryding N, Tufvesson G, Nilsson S (1971) Serum-monoamine-oxidase levels during levodopa therapy. Lancet i: 859.CrossRefGoogle Scholar
  18. Tyce GM, Rorie DK (1982) Conjugated dopamine in superfusates of slices of rat striatum. J Neurochem 39: 1333–1339.PubMedCrossRefGoogle Scholar
  19. Weiss JL, Cohn CK, Chase TN (1971) Reduction of catechol-O-methyltransferase activity by chronic L-dopa therapy. Nature 234: 218–219.PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag 1990

Authors and Affiliations

  • G. M. Tyce
    • 1
    • 3
  • M. K. Dousa
    • 1
  • M. D. Muenter
    • 2
  1. 1.Department of Physiology and BiophysicsMayo Clinic and Mayo FoundationRochesterUSA
  2. 2.Section of NeurologyMayo Clinic ScottsdaleScottsdaleUSA
  3. 3.Department of Physiology and BiophysicsMayo ClinicRochesterUSA

Personalised recommendations