scholarly journals 4-Aminobutyrate in mammalian putrescine catabolism

1975 ◽  
Vol 152 (2) ◽  
pp. 201-210 ◽  
Author(s):  
N. Seiler ◽  
B. Eichentopf
Keyword(s):  
Monoamine Oxidase ◽  
Diamine Oxidase ◽  
Monoamine Oxidase Inhibitor ◽  
Mitochondrial Pathway ◽  
Oxidase Inhibitor ◽  
Catabolic Pathway ◽  
Oxidative Deamination ◽  
Aminobutyrate Aminotransferase ◽  
Derivatives Of

The effects of inhibitors of diamine oxidase (EC 1.4.3.6), monoamine oxidase (EC 1.4.3.4) and 4-aminobutyrate aminotransferase (EC 2.6.1.19) on the catabolism of putrescine in mice in vivo were studied. Diamine oxidase inhibitors and carboxymethoxylamine (amino-oxyacetate) markedly inhibit the metabolism of [14C]putrescine to 14CO2, but affect different enzymes. Aminoguanidine specifically inhibits the mitochondrial and non-mitochondrial diamine oxidases, whereas carboxymethoxylamine specifically inhibits 4-aminobutyrate transamination by the mitochondrial pathway. Hydrazine inhibits at both sites, and results in increased concentrations of 4-aminobutyrate in brain and liver. Pretreatment of mice with carboxymethoxylamine and [14C]putrescine leads to the urinary excretion of amino[14C]butyrate. Carboxymethoxylamine does not affect the non-mitochondrial pathway of putrescine catabolism, as the product of oxidative deamination of putrescine in the extramitochondrial compartment is not further oxidized but is excreted in the urine as derivatives of 4-aminobutyraldehyde. Another catabolic pathway of putrescine involves monoamine oxidase, and the monoamine oxidase inhibitor, pargyline, decreases the metabolism of [14C]putrescine to 14CO2in vivo. Catabolism of putrescine to CO2in vivo occurs along different pathways, both of which have 4-aminobutyrate as a common intermediate, in contrast with the non-mitochondrial catabolism of putrescine, which terminates in the excretion of 4-aminobutyraldehyde derivatives. The significance of the different pathways is discussed.

Biosynthesis of Cerebral Phenolic Amines. I. In Vivo Formation of p-Tyramine, Octopamine, and Synephrine

1972 ◽  
Vol 50 (3) ◽  
pp. 261-267 ◽  
Author(s):  
Alan A. Boulton ◽  
P. H. Wu
Keyword(s):  
Monoamine Oxidase ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor ◽  
Intraventricular Injection

Following the intraventricular injection of 14C-labelled dopamine, p-tyrosine, and p-tyramine to rats pretreated with a monoamine oxidase inhibitor, the labelled phenolic amines p-tyramine, octopamine, and synephrine were isolated and identified as their DNS derivatives. Differences in the amounts of the phenolicamines formed suggest that mechanisms other than just decarboxylation are involved.

scholarly journals Putrescine catabolism in mammalian brain

1974 ◽  
Vol 144 (1) ◽  
pp. 29-35 ◽  
Author(s):  
N. Seiler ◽  
M. J. Al-Therib
Keyword(s):  
Monoamine Oxidase ◽  
Diamine Oxidase ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Mammalian Brain ◽  
Oxidative Deamination ◽  
Acid Cycle ◽  
Degradative Pathway

In contrast with putrescine (1,4-diaminobutane), which is a substrate of diamine oxidase, monoacetylputrescine is oxidatively deaminated both in vitro and in vivo by monoamine oxidase. The product of this reaction is N-acetyl-γ-aminobutyrate. The existence of a degradative pathway in mammalian brain for putrescine is shown, which comprises acetylation of putrescine, oxidative deamination of monoacetylputrescine to N-acetyl-γ-aminobutyrate, transformation of N-acetyl-γ-aminobutyrate to γ-aminobutyrate and degradation of γ-aminobutyrate to CO2 via the tricarboxylic acid cycle.

Urinary Catecholamine Metabolite and Tribulin Output During Lactate Infusion

1988 ◽  
Vol 152 (1) ◽  
pp. 122-126 ◽  
Author(s):  
Angela Clow ◽  
Vivette Glover ◽  
M. W. Weg ◽  
P. L. Walker ◽  
D. V. Sheehan ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Homovanillic Acid ◽  
Monoamine Oxidase Inhibitor ◽  
Benzodiazepine Receptor ◽  
Oxidase Inhibitor ◽  
Panic Attacks ◽  
Urinary Catecholamine ◽  
Lactate Infusion ◽  
Normal Controls

Urinary output of homovanillic acid and 4-hydroxy-3-methoxymandelic acid was decreased both in patients with panic attacks and in normal controls during lactate infusion, whereas that of tribulin (an endogenous monoamine oxidase inhibitor and benzodiazepine receptor binding inhibitor) was increased. There was no change in urinary excretion of any of these compounds during saline infusion. These findings provide further evidence of a link between tribulin output and stress and anxiety in man and point to its possible in vivo action as a monoamine oxidase inhibitor.

scholarly journals The conjugation of tyramine with sulphate by liver and intestine of different animals

1976 ◽  
Vol 160 (3) ◽  
pp. 491-493 ◽  
Author(s):  
K P Wong
Keyword(s):  
Monoamine Oxidase ◽  
Guinea Pig ◽  
Enzyme Preparation ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor ◽  
Oxidative Deamination ◽  
Radioactive Precursor ◽  
Monkey Liver ◽  
Hydroxyphenylacetic Acid ◽  
Low Activity

Tyramine was conjugated with sulphate by extracts of monkey intestine and livers of monkey, rat, mouse, guinea pig and man. The activity measured in monkey intestine was almost three times that of monkey liver. Labelled tyramine sulphate synthesized from [14C] tyramine, [3H] tyramine or Na235SO4, on acid hydrolysis, released its radioactive precursor. Liver extracts of monkey, rat, mouse and guinea pig synthesized respectively 145,66,21 and 6 pmol of [14C] tyramine sulphate/min per mg of protein. Except with the monkey, intestine exhibited very low activity. trans-2-Phenylcyclopropylamine, a monoamine oxidase inhibitor, was added as a routine to the enzyme preparation, as its omission resulted in the production of p-hydroxyphenylacetic acid in appreciable amounts. This oxidative deamination of tyramine, however, did not decrease the sulpho-conjugation of tyramine. The low Km (9.1 μM) of sulphotransferase for tyramine is probably responsible.

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