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Journal of Pharmacology And Experimental Therapeutics, Vol. 174, Issue 3, 401-412, 1970
Copyright © 1970 by American Society for Pharmacology and Experimental Therapeutics

AUGMENTATION OF ALKALOID FORMATION FROM DOPAMINE BY ALCOHOL AND ACETALDEHYDE IN VITRO

Virginia E. Davis 1, Michael J. Walsh 1, and Yasumitsu Yamanaka 1

1 Metabolic Research Laboratory, Veterans Administration Hospital and Department of Biochemistry, Baylor College of Medicine, Houston, Texas

The production of tetrahydropapaveroline (THP), a benzyltetra hydroisoquinoline alkaloid formed by condensation of dopamine and its corresponding aldehyde, is augmented by ethanol and acetaldehyde in vitro. With rat liver homogenates, in the absence of exogenous nicotinamide adenine dinucleotide, ethanol (100 mM) caused a decrease in THP production. The inhibition of THP formation by ethanol was due to promotion of the 3,4-dihydroxyphenylethanol pathway. Acetaldehyde depressed THP generation due to the removal of the substrate by formation of another simple tetrahydroisoquinoline derivative, salsolinol. Salsolinol is an alkaloid formed by condensation of acetaldehyde and dopamine. However, when nicotinamide adenine dinucleotide was added to rat liver homogenates, acetaldehyde (0.5-4.0 mM) significantly decreased the formation of 3,4-dihydroxyphenylacetic acid and concurrently facilitated increased formation of THP. When rat brainstem homogenates were insubated with ethanol or acetaldehyde, 3,4-dihydroxyphenylacetic acid formation was markedly inhibited, whereas THP production was significantly enhanced. These data suggest that ethanol-induced and acetaldehyde-mediated modification of dopamine metabolism with the resultant formation of a benzyltetrahydroisoquinoline alkaloid may contribute to the pharmacologic effects of alcohol, Accordingly, a biochemical concept for the role of neuroamines in the addiction liability of alcohol is advanced.

Submitted on November 13, 1969
Accepted on May 10, 1970




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