Is there an increase in monoamine-oxidase activity in depressive illness?
In a group of depressed patients who had either been treated with or considered suitable for monoamine oxidase (M.A.O.) inhibitor therapy, a highly significant decrease in conjugated tyramine output was observed after an oral tyramine load compared with normal controls. However, there was no difference in conjugated isoprenaline output between the two groups after isoprenaline ingestion, even though this amine is almost solely metabolised by what is likely to be the same conjugation mechanism. Whilst some explanation in terms of altered gut motility is conceivable, it seems more likely that the apparent deficit in tyramine conjugation in depression represents an increase in functional M.A.O. activity. Consequently, this enzyme would metabolise a greater proportion of available amine, causing a proportionately large decrease in the smaller conjugate pool.
D000284:Administration, Oral; D000328:Adult; D000368:Aged; D002940:Circadian Rhythm; D003863:Depression / Q000188:drug therapy / Q000201:enzymology* / Q000378:metabolism; D006801:Humans; D007490:Iproniazid / Q000627:therapeutic use; D007545:Isoproterenol / Q000008:administration & dosage / Q000652:urine; D008875:Middle Aged; D008995:Monoamine Oxidase / Q000378:metabolism*; D013997:Time Factors; D014439:Tyramine / Q000008:administration & dosage / Q000378:metabolism / Q000652:urine
D007490:Iproniazid; D008995:Monoamine Oxidase; D007545:Isoproterenol; D014439:Tyramine