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At least 667 records · Page 37Linked to original sources
PubMed1997

Pharmacology of the new reversible inhibitor of monoamine oxidase A, RS-8359.

RS-8359 is a new reversible inhibitor of monoamine oxidase A (RIMA). With a selectivity ratio of about 2200 for the A:B enzyme types, it is one of the most specific of this class of compounds. As a result, it shows relatively little effect upon blood pressure when administered together with tyramine, thus effectively eliminating the 'cheese' effect which has contributed to the limited clinical use of the classical monoamine oxidase inhibitors (MAOIs). RS-8359 shows little affinity for the common central nervous system receptors and little anticholinergic effect. These characteristics suggest a relatively benign adverse event profile, which may be particularly advantageous in the elderly and may generally contribute to patient acceptance and compliance. In terms of its effects upon serotonin (5-hydroxytryptamine), RS-8359 gives increases similar to those of other MAOIs with activity sustained for about 9 h. In behavioural investigations, the compound gives results similar to those found with several antidepressants widely used in the clinic. Overall, the pharmacology of RS-8359 indicates that it should have antidepressant activity in man.

Animals↗
PubMedDate not supplied

Isolation and characterization of monoamine oxidase from hyperfunctioning human thyroid.

Human thyroid monoamine oxidase from hyperfunctioning thyroids was isolated and purified by separating the mitochondria by differential centrifugation followed by ultrasonication. The suspension containing the active enzyme from the DEAE-column, on passing through a Sephadex G-200 column gave three peaks corresponding to molecular weights of approximately 220,000, 23,000 and 4000 of which the component with molecular weight 4000 showed enzyme activity. The blood of the patients was analyzed for plasma MAO, RBC cholinesterase, plasma histaminase and plasma catecholamines. Histology and histochemistry of the thyroid tissues were also done. The data are examined from the point of view of the prevalent idea of the possible existence of MAO in multiple forms.

Adolescent↗
PubMed1978

The influence of L-tryptophan and monoamine oxidase inhibitors on catecholamine metabolism in rat brain.

1. L-Tryptophan (100 mg/kg) was administered to rats with or without pretreatment with a monoamine oxidase inhibitor and the concentration of 5-hydroxyindoleacetic acid, homovanillic acid, dihydroxyphenylacetic acid, 3-methoxy 4-hydroxyphenyl glycol, normetanephrine, noradrenaline and dopamine measured in whole brain one hour later. 2. L-Tryptophan increased the concentration of 5-hydroxyindoleacetic acid, homovanillic acid, dihydroxyphenylacetic acid, 3-methoxy 4-hydroxyphenyl glycol and normetanephrine. The concentration of noradrenaline did not change whilst that of dopamine increased significantly. 3. In animals pretreated chronically with a monoamine oxidase inhibitor, tryptophan increased the concentration of dihydroxyphenylacetic acid and homovanillic acid compared to monoamine oxidase alone. 4. The results suggest either a release of dopamine and noradrenaline by 5-hydroxytryptamine, with a compensatory increase in their synthesis, or an increase in the firing of dopaminergic and noradrenergic neurones after L-tryptophan.

Animals↗
PubMed1983

The diagnostic potential of the combined determination of serum monoamine oxidase and N-acetyl-beta-D-glucosaminidase for fibroproliferative liver diseases.

The simultaneous determination of the catalytic activities in serum of monoamine oxidase (EC 1.4.3.4) and N-acetyl-beta-D-glucosaminidase (EC 3.2.1.30) was performed in patients with various non-liver diseases, acute hepatitis and fibroproliferative liver disorders (cirrhosis and fibrosis) and the predictive values of the positive (both activities are pathologically elevated) and negative test results (normal activity of monoamine oxidase and/or N-acetyl-beta-D-glucosaminidase) were estimated. It was found that the incidence of the positive result is extremely low (0.024, 5/207) in patients suffering from a great variety of non-liver and liver diseases (except cirrhosis) but rather great in liver cirrhotic subjects (0.44, 18/41). A fraction of only 0.07 of liver fibrotic patients had a positive test result. Based on these data the estimated predictive value of the positive result for liver cirrhosis at a prevalence of 0.03 is 0.47. This value increases strongly with higher prevalence of cirrhosis (population preselected for chronic liver diseases). The negative predictive value for cirrhosis and the positive value for fibrosis are low. Thus, the probability of the presence of cirrhosis in patients with suspected chronic liver diseases is great in cases of abnormally high activities of both monoamine oxidase and N-acetyl-beta-D-glucosaminidase. Negative test results (normal catalytic activities of one or both enzymes), however, do not prove the absence of liver cirrhosis and/or liver fibrosis.

Acetylglucosaminidase↗
PubMed1979

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.

Animals↗
PubMed1996

Observation of a flavin semiquinone in the resting state of monoamine oxidase B by electron paramagnetic resonance and electron nuclear double resonance spectroscopy.

Monoamine oxidase (MAO) plays an essential role in the regulation of various neurotransmitter and xenobiotic amines. Inhibitors of MAO have been employed in the treatment of depression and as adjuncts in Parkinson's disease therapy. X-Band and Q-band electron paramagnetic resonance (EPR) and electron nuclear double resonance (ENDOR) spectroscopic techniques are employed to characterize a signal assigned as a stable red anionic semiquinone radical in the resting state of MAO B. It is shown that the radical signal is not affected during substrate (either benzylamine or phenylethylamine) turnover, by anaerobic incubation with substrate, or by covalent modification of the active site flavin cofactor in the catalytically active dimer. Upon denaturation, however, the semiquinone absorbances and EPR signals are lost. Photoreduction of the native enzyme in the presence of ethylenediaminetetraacetate generates an EPR signal that is not the same as that obtained in the resting state and shows different proton ENDOR signals. These results suggest that the two flavin prosthetic groups that exist in catalytically active monoamine oxidase B are physically distinct.

Animals↗
PubMed1975

In vitro inhibition of brain mitochondrial monoamine oxidase by 6-hydroxydopamine.

6-Hydroxydopamine (6-OHDA) inhibits rat brain mitochondrial monoamine oxidase (MAO) when kynuramine or dopamine are used as substrates. The effect is competitive and reversible giving Ki values of 74 and 176 muM with the respective substrates. At high concentrations (5 mM) of each substrate, inhibition of MAO was not observed.

Animals↗
PubMed2000

Comparison of neurochemical effects of the monoamine oxidase inhibitors phenelzine, moclobemide and brofaromine in the rat after short- and long-term administration.

BACKGROUND: Chronic administration of several irreversible monoamine oxidase (MAO) inhibitors induces a down-regulation of tryptamine and 5-hydroxytryptamine(2) receptors in rat brain, but there is a paucity of information available on the effects of reversible MAO-A inhibitors on these receptors. METHODS: Acute and chronic experiments were conducted in rats and the effects of the irreversible monoamine oxidase inhibitor, phenelzine and the reversible MAO type-A inhibitors, moclobemide and brofaromine, on tryptamine and 5-hydroxytryptamine(2) receptors were analysed using radioligand binding techniques. In addition, activities of MAO-A and -B were determined radiochemically and brain and/or urine levels of tryptamine, 5-hydroxytryptamine, 3-methoxy-4-hydroxyphenylglycol (MHPG), beta-phenylethylamine, brofaromine and moclobemide were determined by chromatographic procedures. RESULTS: After 30 days of administration, moclobemide and brofaromine selectively inhibited brain MAO-A activity and phenelzine inhibited MAO-A and -B to equal extents. All three drugs caused a significant down-regulation of tryptamine receptors, whereas only phenelzine significantly down-regulated 5-hydroxytryptamine(2) receptors. In a comparison of phenelzine and brofaromine, both caused marked elevations of urinary tryptamine and decreases of urinary MHPG levels, while only phenelzine increased beta-phenylethylamine levels. After 14 days of administration, phenelzine, but not moclobemide or brofaromine, significantly increased levels of tryptamine in brain; all three drugs significantly increased 5-HT levels. LIMITATIONS: 24-h urine samples were not collected for moclobemide-treated animals and brain levels of tryptamine were not measured after 30-day administration. CONCLUSIONS: These studies revealed marked neurochemical differences among phenelzine, moclobemide and brofaromine which could contribute to their actions in the clinical setting.

Animals↗
PubMedDate not supplied

[Properties of monoamine oxidase in the brain of mongolian gerbils during cerebral ischemia].

Properties of monoamine oxidase (MAO) were investigated in mongolian gerbils brain mitochondria isolated from cerebral cortex, striatum and hippocampus during cerebral ischemia. 5 min of ischemia caused inhibition of MAO activity (kynuramine as a substrate), alterations in substrate specificity and in kinetic curves form deflexion from hyperbolic type in all the brain structures investigated. Alterations in properties of MAO were observed in hippocampus already after I min of ischemia.

Animals↗
PubMed2006

Increased monoamine oxidase and semicarbazide-sensitive amine oxidase activities in white adipose tissue of obese dogs fed a high-fat diet.

Adipocytes express two types of amine oxidases: the cell surface semicarbazide-sensitive amine oxidase (SSAO) and the mitochondrial monoamine oxidase (MAO). In human abdominal subcutaneous adipose tissue, it has been reported that SSAO substrates stimulate glucose transport and inhibit lipolysis while MAO activity is decreased in obese patients when compared to age-matched controls. However, no information has been reported on visceral WAT. To further investigate the obesity-induced regulations of MAO and SSAO in white adipose tissue (WAT) from different anatomical locations, enzyme activities and mRNA abundance have been determined on tissue biopsies from control and high-fat fed dogs, an obesity model already described to be associated with arterial hypertension and hyperinsulinemia. MAO activity was increased in the enlarged omental WAT of diet-induced obese dogs, but not in their mesenteric WAT, another intra-abdominal fat depot. Subcutaneous WAT did not exhibit any change in MAO activity, as did the richest MAO-containing tissue: liver. Similarly, SSAO was increased in omental WAT of diet-induced obese dogs, but was not modified in other WAT and in aorta. The increase in SSAO activity observed in omental WAT likely results from an increased expression of the AOC3 gene since mRNA abundance and maximal benzylamine oxidation velocity were increased. Finally, plasma SSAO was decreased in obese dogs. Although the observed regulations differ from those found in subcutaneous WAT of obese patients, this canine model shows a tissue- and site-specific regulation of peripheral MAO and SSAO in obesity.

Adipose Tissue, White↗
PubMed1978

Multiple forms of monoamine oxidase in developing chick brain.

The developmental change in the multiplicity of monoamine oxidase (MAO) forms of chick brain was studied with regard to substrate specificity and inhibitor sensitivity. The developmental pattern of MAO activity towards beta-phenylethylamine was generally similar to that of MAO activity towards 5-hydroxytryptamine. The inhibition study showed that the ratio of type A MAO to type B MAO in chick brain increased during development. This is quite different from results obtained in mice, rats, guinea pigs, and humans, and is not consistent with the idea that in immature brain type A MAO predominates.

Animals↗
PubMed1979

Variations in mitochondrial monoamine oxidase during progressive starvation in the brain of developing rats.

Effects of progressive starvation of 12, 24, 48 and 60 h upon brain mitochondrial monoamine oxidase activity were studied. The enzyme activity was determined by three different substrates: 14C-labeled tryptamine, dopamine and kynuramine. With dopamine as substrate, the enzyme activity showed decline during 24 and 48 h of starvation. Monoamine oxidase when determined by tryptamine as the substrate, showed a decrease after 60 h of starvation. The use of kynuramine as substrate also produced a decrease in enzyme activity after 48 and 60 h of starvation. Refeeding the 60-h-starved rats for the following 24 h resulted in further decrease of monoamine oxidase activity of brain mitochondria from the 60 h starved values. The results suggest that oxidative deamination of biogenic amines is greatly inhibited during progressive starvation and remains low even after feeding the 60 h starved rats for 24 h.

Animals↗
PubMed2006

Immobilization stress increases endogenous monoamine oxidase (MAO) inhibitor in rat liver.

Although the physiological role of endogenous monoamine oxidase (MAO) inhibitor still remains unclear, the present study examined whether or not immobilization stress (IMMO) induce MAO inhibitor. An endogenous inhibitor of MAO was separated by gel filtration from 105,000 g supernate in rat liver cytosol following IMMO. The molecular weight of this inhibitor was estimated to be 500-600 by gel filtration. This inhibitor was proved to be heat-stable resistant to protease treatment. IMMO for 2 h significantly decreased MAO. These results suggest that this inhibitor is induced by IMMO. MAO activity in rat liver might be regulated by the level of this inhibitor.

Animals↗
PubMed2005

Monoamine oxidase inhibitory components from the roots of Sophora flavescens.

In our search for monoamine oxidase (MAO) inhibitors from natural resources, we found that the methanol extract of the roots of Sophora flavescens showed an inhibitory effect on mouse brain monoamine oxidase (MAO). Bioactivity-guided isolation of the extract yielded two known flavonoids, formononetin (1) and kushenol F (2), as active compounds along with three inactive compounds, oxymatrine (3), trifolirhizin (4), and beta-sitosterol (5). Formononetin (1) and kushenol F (2) showed significant inhibitory effects on MAO in a dose-dependent manner with IC50 values of 13.2 and 69.9 microM, respectively. Formononetin (1) showed a slightly more potent inhibitory effect against MAO-B (IC50: 11.0 microM) than MAO-A (IC50: 21.2 microM). Kushenol F (2) also preferentially inhibited the MAO-B activity than MAO-A activity with the IC50 values of 63.1 and 103.7 microM, respectively.

Animals↗
PubMed1981

Alteration of dopamine synthesis in rat striatum subsequent to selective type A monoamine oxidase inhibition.

Pretreatment of rat striatal slices with the selective type A monoamine oxidase (MAO) inhibitor clorgyline was found to produce significant inhibition of dopamine (DA) synthesis. DA synthesis was reduced by nearly 50%, but not until more than 90% of the type A enzyme was inhibited. In contrast, complete inhibition of the type B MAO following deprenyl treatment had no effect. It is suggested that interneuronal accumulation of DA following inhibition of type A MAO leads to feedback inhibition at the rate-limiting step in DA biosynthesis, tyrosine hydroxylation. These results are also consistent with the presence of a type A MAO within DA-containing neurons and provide evidence of a regulatory role for type A MAO in the synthesis of brain DA.

Animals↗
PubMed1989

Potentiation of para-hydroxyamphetamine-induced head-twitch response by inhibition of monoamine oxidase type A in the brain.

After pretreatment with either clorgyline, a monoamine oxidase (MAO)-A-selective inhibitor, or pargyline, an MAO-B-selective inhibitor with less selectivity than l-deprenyl, i.c.v. administration of para-hydroxyamphetamine (p-OHA) significantly increased both the frequency and total number of head-twitches in mice. A typical MAO-B-selective inhibitor, l-deprenyl, however, did not change the total count of the p-OHA-induced head-twitch response (HTR). These effects were also found with fixed doses of the selective MAO inhibitors when p-OHA was varied. Administration of clorgyline (1 mg/kg) or pargyline (5 mg/kg) almost inhibited completely MAO-A in the mouse forebrain, and pargyline also almost inhibited completely MAO-B. l-Deprenyl, in contrast, almost inhibited completely MAO-B without affecting MAO-A activity. Systemic administration of l-5-hydroxytryptophan also induced HTR and the total number of twitches was enhanced by clorgyline, but not by pargyline or l-deprenyl. Chlorimipramine or cocaine significantly reduced p-OHA-induced HTR, suggesting an intraneuronal site of action. Together with the presence of considerable MAO-A in 5-hydroxytryptamine (5-HT) neurons of various animal species, and possible accumulation and subsequent monoamine-releasing properties of p-OHA, the present results indicate that p-OHA might induce the HTR by interaction with intraneuronally increased 5-HT. This mechanism probably results in 5-HT release onto the postsynaptic 5-HT2 receptors. Taken together, different roles of MAO-B in "the hyperactivity syndrome" and the HTR are discussed.

Amphetamines↗