HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Karoum, F. Articles by Wyatt, R. J. Search for Related Content PubMed PubMed Citation Articles by Karoum, F. Articles by Wyatt, R. J.

Metabolism of (-) deprenyl to amphetamine and methamphetamine may be responsible for deprenyl's therapeutic benefit

A biochemical assessment

Adult Psychiatry Branch (Drs. Karoum and Wyatt and Ms. Chuang), Division of Special Mental Health Research, National Institute of Mental Health, Saint Elizabeths Hospital, Washington, D.C., the Experimental Therapeutics Branch, National Insititute of Neurological and Communicative Disorders and Stroke, National Institutes of Health (Drs. Eisler and Calne), Bethesda, MD, and the Department of Mental Hygiene, New York State Psychiatric Institute (Drs. Liebowitz, Quitkin, and Klein), New York, NY.

The urinary excretion of some important phenylethylamines, catecholamines, their metabolites, amphetamine, and methamphetamine were measured in parkinsonian patients on Sinemet (L-dopa plus carbidopa, a peripheral dopadecarboxylase inhibitor) and depressed patients after chronic (-) deprenyl treatment. Deprenyl was efficiently metabolized to amphetamine and methamphetamine. It increased the excretion of phenylethylamine and of m-and p-tyramine, and reduced the output of norepinephrine metabolites, but failed to alter the excretion of dopamine-deaminated metabolites. These changes were attributed more to amphetamine and methamphetamine than to inhibition of monoamine oxidase type B. Sinemet treatment alone increased the excretion of dopamine, 3-methoxytyramine, and their respective deaminated metabolites, 3, 4-dihydroxyphenylacetic acid and homovanillic acid. It is concluded that conversion of deprenyl to amphetamine and methamphetamine may contribute to some of the therapeutic benefits of deprenyl.

Address correspondence and reprint requests to Dr. Karoum, Adult Psychiatry Branch, Division of Special Mental Health Research, National Institute of Mental Health, Saint Elizabeths Hospital, Washington, D.C. 20032.

Accepted for publication September 1, 1981.

This article has been cited by other articles:

				H. K. Wayment, J. O. Schenk, and B. A. Sorg Characterization of Extracellular Dopamine Clearance in the Medial Prefrontal Cortex: Role of Monoamine Uptake and Monoamine Oxidase Inhibition J. Neurosci., January 1, 2001; 21(1): 35 - 44. [Abstract] [Full Text] [PDF]

				D. A. Durden, L. E. Dyck, B. A. Davis, Y.-D. Liu, and A. A. Boulton Metabolism and Pharmacokinetics, in the Rat, of (R)-N-(2-Heptyl)Methyl-Propargylamine (R-2HMP), A New Potent Monoamine Oxidase Inhibitor and Antiapoptotic Agent Drug Metab. Dispos., February 1, 2000; 28(2): 147 - 154. [Abstract] [Full Text]

				G. W. Carlile, R. M. E. Chalmers-Redman, N. A. Tatton, A. Pong, K. E. Borden, and W. G. Tatton Reduced Apoptosis after Nerve Growth Factor and Serum Withdrawal: Conversion of Tetrameric Glyceraldehyde-3-Phosphate Dehydrogenase to a Dimer Mol. Pharmacol., January 1, 2000; 57(1): 2 - 12. [Abstract] [Full Text]