Abstract
HYPNOTIC doses of ethanol have been reported by Rosenfeld1 to prolong the metabolic inactivation of exogenous serotonin (5-hydroxytryptamine) in mice. Olson, Gursey, and Vester2 found the urinary excretion of 5-hydroxyindolylacetic acid (5–HIAA) to be significantly below normal in alcoholics, even after 6 months of abstinence on rigidly controlled diets. These findings suggest that ethanol may act as a monoamine oxidase (MAO) inhibitor. On the other hand, Gursey and Olson3 have reported depression of brain-stem serotonin and norepinephrine in rabbits after both acute and chronic ethanol administration; suggesting that ethanol may act to release stores of bound amines. Pscheidt, Issekutz, and Himwich4 were unable to confirm this finding. In our laboratories, we have found that a single dose of ethanol, given orally to human volunteers, produces a marked, but transitory, increase in the urinary excretion of tryptamine5.
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References
Rosenfeld, G., Proc. Soc. Exp. Biol. Med., 103, 144 (1960).
Olson, R. E., Gursey, D., and Vester, J. W., New England J. Med., 263, 1169 (1960).
Gursey, D., and Olson, R. E., Proc. Soc. Exp. Biol. Med., 104, 280 (1960).
Pscheidt, G. R., Issekutz, B., and Himwich, H. E., Quart. J. Studies on Alcohol., 22, 550 (1961).
Schenker, V. J., Maynard, L. S., and Rothrock, I., Proc. Nat. Counc. on Alcoholism Symp., Biochemical Factors in Alcoholism (in the press).
Westerfeld, W. W., and Schulman, M. P., Quart. J. Studies on Alcohol, 20, 439 (1959).
Udenfriend, S., Weissbach, H., and Clark, C. T., J. Biol. Chem., 215, 337 (1955).
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MAYNARD, L., SCHENKER, V. Monoamine Oxidase Inhibition by Ethanol in vitro. Nature 196, 575–576 (1962). https://doi.org/10.1038/196575a0
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DOI: https://doi.org/10.1038/196575a0
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