The effect of monoamine oxidase inhibitors on conjugation

Zusammenfassung Die Wirkung von Monoamino-Oxidase-Blockern in Verbindungen ist in vitro veränderlich und hängt vom benutzten Substrat und Gewebe ab. Im allgemeinen wird dieo-Aminophenol-Verbindung blockiert, während die Bilirubinverbindung verhindert oder auch angeregt werden kann. Die verschiedenen Wirkungen können von Variationen von der Verfügbarkeit des Substrats für die Enzyme abhängen. Es ist sehr unwahrscheinlich, dass die Monoamino-Oxidase-Blocker-Gelbsucht aus der Blockierung der Glucuronyl-Transferase allein zu erklären ist.     

Effect of some monoamine oxidase inhibitors on deamination of biogenic monoamines by rat liver mitochondrial monoamine oxidase

N--N- MAO , , .     

Increase of pyruvic and lactic acid in rat blood by inhibitors of monoamine oxidase

Zusammenfassung Monoaminoxydase(MAO)-Hemmer verschiedener chemischer Klassen sowie Monoamin-Freisetzer erhöhen den Milch- und Brenztraubensäuregehalt im Rattenblut. Der zeitliche Verlauf dieser Vermehrung verhält sich ähnlich wie die 5-Hydroxytryptamin-Akkumulation bzw. -Freisetzung im Gehirn. Im weiteren verstärkt der MAO-Hemmer Iproniazid den durch 5-Hydroxytryptamin oder Noradrenalin bedingten Anstieg von Milch- und Brenztraubensäure im Blut.     

Affinity chromatography of monoamine oxidase

Summary A method is described for the purification of pig liver monoamine oxidase by affinity chromatography, using a colum with covalently bound pargyline.Acknowledgment. The authors wish to thank the University Research Council for financial support.     

Antagonism between harmaline and long-acting monoamine oxidase inhibitors concerning the effect on 5-hydroxytryptamine and norepinephrine metabolism in the brain

Zusammenfassung Vorbehandlung mit Harmalin hemmte den Anstieg von 5-Hydroxytryptamin (5HT) und Noradrenalin (NE) im Gehirn von Ratten und Mäusen, welcher durch zwei lang-dauernd wirkende Monoaminoxydasehemmer verursacht wurde (Isopropylhydrazide von Isonikotinsäure und -Isopropylhydrazid von Glutaminsäure). Wurde Harmalin 6–8 h nach den Hydraziden appliziert, so konnte kein Absinken des durch das Hydrazid erhöhten Monoamin-Gehaltes beobachtet werden. Mit Hilfe dieses Antagonismus zwischen Harmalin und Hydraziden dürfte es möglich sein, mehr Kenntnis über die Rolle der Monoaminoxydase bei der Wirkung von Pharmaka zu gewinnen.     

Chlorodimeform and its effect on monoamine oxidase activity in the cattle tickBoophilus microplus

Summary The action of the acaricide, chlorodimeform and its metabolite, N-desmethylchlorodimeform, on the activity monoamine oxidase (MAO) from the cattle tick,Boophilus microplus, were studied, Both compounds were found to be potent in vitro and in vivo inhibitors of the enzyme. However the inhibition of MAO does not seem to be related to the toxic action of the acaricide.     

Multiplicity of monoamine oxidase in chick brain

Summary The substrate- and inhibitor-related characteristics of monoamine oxidase (MAO) were studied on chick brain mitochondria. It was found that neither 5-hydroxytryptamine nor -phenylethylamine is the specific substrate for type A and type B MAO in chick brain.     

Occurrence of mitochondrial monoamine oxidase in human semen

Summary Mitochondrial monoamine oxidase (MAO) was found in human semen, showing its K_m and V_max values of 91.7 M and 290 pmoles/mg of protein/60 min, respectively, with kynuramine as substrate. A major part of the activity was due to type A MAO.     

Multiple forms of monoamine oxidase in developing Xenopus

Zusammenfassung Das Isoenzymmuster der Monoaminoxidase verändert sich während der frühen Entwicklung der Larven vonXenopus laevis. Die Anzahl elektrophoretischer Banden verkleinert sich während der Entwicklung von vier auf eine.

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The author was supported by a grant from the Cleveland State University Faculty Research Committee. The author would like to express his thanks toJohn Y. Pun the president of Bionix (El Cerrito, California) for the use of the apparatus.     

Multiplicity of monoamine oxidase in chick brain.

The substrate- and inhibitor-related characteristics of monoamine oxidase (MAO) were studied on chick brain mitochondria. It was found that neither 5-hydroxytryptamine nor beta-phenylethylamine is the specific substrate for type A and type B MAO in chick brain.     

Histochemical studies of monoamine oxidase during axonal reaction

Zusammenfassung Es werden Veränderungen der MAO-Aktivität im Rückenmark oder in der Medulla oblongata von Ratten beschrieben, die durch die Sektion des N. ischiadicus oder des N. hypoglossus verursacht wurden.     

Platelet monoamine oxidase B: Use and misuse

The human platelet in addition to having serotonin (5-HT) receptors, uptake carriers (receptor) and transmitter storage vesicles, primarily possesses mitochondrial monoamine oxidase (MAO) type B. Similar to the major form of MAO in the human brain, this enzyme actively oxidizes A-B and B substrates (tyramine, dopamine, phenylethylamine) as well as the novel secondary amine anticonvulsant, milacemide and dopaminergic neurotoxin, MPTP. 5-HT oxidation is hardly affected by the platelet enzyme and MAO inhibitors have no net effect on its accumulation. MAO-B is selectively inhibited by 1-deprenyl and thus the platelet enzyme may be useful to monitor the anti-Parkinson activity of such drugs, as related to their ability to inhibit brain MAO-B. The oxidation of the anticonvulsant, milacemide, to glycine in vitro and in vivo by MAO-B, may herald new prospects for the development of inert prodrugs capable of being metabolized to neuroactive substances by MAO-B. The plasma levels of their metabolites may be an index of MAO-B activity found in the platelet and brain.     

Platelet monoamine oxidase B: use and misuse

The human platelet in addition to having serotonin (5-HT) receptors, uptake carriers (receptor) and transmitter storage vesicles, primarily possesses mitochondrial monoamine oxidase (MAO) type B. Similar to the major form of MAO in the human brain, this enzyme actively oxidizes A-B and B substrates (tyramine, dopamine, phenylethylamine) as well as the novel secondary amine anticonvulsant, milacemide and dopaminergic neurotoxin, MPTP. 5-HT oxidation is hardly affected by the platelet enzyme and MAO inhibitors have no net effect on its accumulation. MAO-B is selectively inhibited by 1-deprenyl and thus the platelet enzyme may be useful to monitor the anti-Parkinson activity of such drugs, as related to their ability to inhibit brain MAO-B. The oxidation of the anticonvulsant, milacemide, to glycine in vitro and in vivo by MAO-B, may herald new prospects for the development of inert prodrugs capable of being metabolized to neuroactive substances by MAO-B. The plasma levels of their metabolites may be an index of MAO-B activity found in the platelet and brain.