Melatonin: Deacetylation to 5-methoxytryptamine by liver but not brain aryl acylamidase

Michael A Rogawski, R. H. Roth, G. K. Aghajanian

Research output: Contribution to journalArticlepeer-review

53 Scopus citations


Rat liver and brain slices were incubated in vitro with [3H]melatonin. Liver slices synthesized small amounts of [3H]5-methoxyindoleacetic acid [3H]5-MIAA) along with other melatonin metabolites including 6-hydroxymelatonin. Pretreatment of animals prior to killing with the irreversible monoamine oxidase inhibitor pargyline allowed [3H]5-methoxytryptamine ([3H]5-MT) to be recovered from the incubation. No [3H]5-MIAA or [3H]5-MT could be detected in incubations with hypothalamic slices or following intraventricular injection of [3H]melatonin. The possibility that the deacetylase aryl acylamidase was in part responsible for the deacetylation occurring in liver slices was examined. Liver aryl acylamidase was able to utilize [3H]melatonin as substrate to produce [3H]5-MT. Furthermore, the liver enzyme was inhibited by melatonin (K(i) 1 mM) when tested with the alternate substrate o-nitroacetanalide. Brain aryl acylamidase did not generate any detectable [3H]5-MT nor was it inhibited by melatonin. These results suggest that 5-MT is not formed in brain from melatonin although trace amounts of 5-MT in the periphery could be derived from this precursor.

Original languageEnglish (US)
Pages (from-to)1219-1226
Number of pages8
JournalJournal of Neurochemistry
Issue number4
StatePublished - 1979
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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