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Results for “MONOAMINE OXIDASE”

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At least 1,009 records · Page 56Linked to original sources
PubMed1976

Reduced platelet monoamine oxidase activity in a subgroup of schizophrenic patients.

Platelet monoamine oxidase (MAO) activity was significantly lower than control values in a subgroup of 16 schizophrenic patients (most of whom were paranoid) characterized by the presence of auditory hallucinations and delusions. Platelet MAO activity was not reduced in 16 other schizophrenic patients without auditory hallucinations. This finding suggests that reduced platelet MAO activity is not found in all schizophrenic patients but tends to occur in a clinically identifiable subgroup.

Auditory Perception↗
PubMed1989

Endogenous urinary monoamine oxidase inhibitor excretion in Parkinson's disease and other neurological disorders.

In this study, urinary output of both neutral (tribulin) and basic monoamine oxidase inhibitory activity was measured in parkinsonian patients, other neurological patients and controls. No significant differences in output were found between these different groups. In general, tribulin output rose with age, in parallel with known changes in monoamine oxidase B activity.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2004

The role of monoamine oxidase inhibitors in current psychiatric practice.

The use of monoamine oxidase inhibitors (MAOIs) by psychiatrists has declined over the past several decades with the expansion of psychiatrists' pharmacologic armamentarium. This trend has also been driven by concern about food and drug interactions and side effects, as well as waning physician experience with these medications. Many psychiatrists, in fact, never prescribe MAOIs. Recent research has liberalized the MAOI diet and identified symptom presentations more likely to respond to these medications. Thus, clinicians must continue to familiarize themselves with the properties of and indications for prescribing MAOIs.

Depressive Disorder↗
PubMed1978

Clinical correlates of tricyclic antidepressant-mediated inhibition of platelet monoamine oxidase.

Previous reports suggest that tricyclic antidepressants inhibit platelet monoamine oxidase (MAO) activity in vitro and in vivo. This study was undertaken to examine the relationship between tricyclic-mediated inhibition of platelet MAO and resolution of clinical signs and symptoms which are commonly associated with the depressive syndrome. The results indicate that the sedative-hypnotic effects of the tricyclics closely correlate with the magnitude of platelet MAO inhibition. It appears that these effects may be mediated through alterations in the metabolism of serotonin and/or the phenylethylamines.

Adult↗
PubMed1983

Type A and B monoamine oxidase in glial cells in long-term culture.

Monoamine oxidase (MAO) in astroglial primary cultures increased during cell development. The enzyme activity towards type B substrate was further enhanced in cultures treated with 0.25 mM dibutyl cyclic AMP (dBcAMP), although dBcAMP (1 mM) does not effect MAO activity in vitro. It has been estimated that the dBcAMP treated cultures contain 70% type A and 30% type B MAO, while in the untreated one, there was virtually only type A MAO. Following the application of Percoll density gradient centrifugation, MAO associated with different subcellular fractions was obtained. The dBcAMP treated fractions were slightly heavier than the untreated ones.

Animals↗
PubMed1985

Mitochondrial monoamine oxidase activity during preneural developmental stages of Bufo bufo.

Monoamine oxidase specific activities against PEA and 5-HT have been measured in mitochondria isolated from early embryos of Bufo bufo. During the early development up to the neural fold stage, MAO activity undergoes a continuous decrease that is more evident when PEA is used as the substrate. The inhibition patterns of deprenyl and clorgyline demonstrate that, at the neural fold stage, both type A and B MAO are present. Both in eggs and embryos MAO type A activity appears slightly more sensitive to the inhibitory effect of various concentrations (0.1-2 M) of the denaturing agent urea.

Animals↗
PubMed1986

Distribution of endogenous benzodiazepine receptor ligand-monoamine oxidase inhibitory activity (tribulin) in tissues.

The distribution of monoamine oxidase inhibitor-benzodiazepine receptor binding inhibitor, extractable into ethyl acetate at pH 1, was examined in a range of rat tissues. Great variation in the activity of both inhibitors was found in the different tissues, the highest being present in superior cervical ganglion, and lowest in adrenal gland. There was a highly significant correlation between the distribution of the two activities in different tissues, supporting the concept that they both derive from the same molecule (tribulin). The level of inhibitory activity in some of the tissues was such that variations might conceivably play a significant role in vivo.

Animals↗
PubMedDate not supplied

[Kinetic properties of monoamine oxidase isoenzymes from the bovine brain].

Multiple forms of monoamine oxidase (MAO I, IIa, IIb, III) from bovine brain, separated by means of affinity chromatography on AH-Sepharose 4B, were dissimilar in kinetics of deamination of serotonin and beta-phenylethylamine used as substrates of the MAO of A and B types. MAO-I catalyzed the deamination of beta-phenyl ethylamine and serotonin. Km and Vmax values could not be calculated for MAO-IIa since the rate of enzymatic reactions was characterized by a complicated dependence on concentration of serotonin in a sample. MAO-IIb catalyzed also the deamination of both AMO substrates.

2-Hydroxyphenethylamine↗
PubMed1977

Platelet monoamine oxidase activity in schizophrenic patients.

The authors studied platelet monoamine oxidase (MAO) activity in 29 schizophrenic inpatients and 26 schizophrenic outpatients during a 4-week double-blind trial of chlorpromazine with imipramine or thiothixene with placebo. The found that significantly more schizophrenic patients than normal control subjects had low platelet MAO activity after 4 weeks. Outpatients with low MAO activity were distinguished by increased behavioral activity and reduced social apathy. Inpatients with low MAO activity were distinguished by severity of illness and symptoms. Hallucinations were significantly more frequent among patients with low MAO activity. The authors suggest that platelet MAO activity might decline in some actively schizophrenic patients as part of the psychotic process.

Ambulatory Care↗
PubMed1991

Monoamine oxidase, dopamine and Parkinson's disease.

Four aspects about monoamine oxidase (MAO; E.C. 1.4.3.4) are of obvious interest in relation to Parkinson's disease and its treatment with the irreversible and selective MAO-B inhibitor L-deprenyl and are discussed in this review: 1) To what extent the two forms of MAO are of importance for the deamination of dopamine and to what degree MAO localised inside and outside of dopaminergic nerve terminals contributes 2) The kinetics of the MAO-protein, i.e. the rate of recovery of MAO after irreversible inhibition. 3) To what extent MAO may be changed as a consequence of the pathophysiological processes. 4) To what extent MAO may be involved as a force in the pathophysiological processes.

Animals↗
PubMed1984

Platelet monoamine oxidase response to lithium treatment in psychiatric patients.

Platelet monoamine oxidase (MAO) activity was studied in bipolar and schizophrenic patients treated with lithium and was found to be increased as a nonspecific drug effect. Greater MAO increase in manic patients was correlated with lesser clinical improvement. There was no correlation of MAO activity with short-term outcome in schizophrenic patients. Change in MAO was not correlated with lithium dosage or plasma levels. Patients with baseline MAO values below the median had the largest activity increases. Platelet MAO might thus be characterized as a state variable, increased by lithium as a nonspecific pharmacologic effect, with the increase associated with poor clinical outcome in manic patients.

Adult↗
PubMed1997

Continuation and maintenance treatments in major depression: the neglected role of monoamine oxidase inhibitors.

The importance of continuation and maintenance antidepressant therapy has been increasingly recognized, but usually focuses on tricyclic and selective serotonin reuptake inhibitor (SSRI) antidepressants. This review examines the evidence in support of classical monoamine oxidase inhibitor (MAOI) agents and the selective reversible monoamine oxidase type A inhibitor moclobemide in continuation and maintenance therapy. Phenelzine and tranylcypromine have demonstrated long-term efficacy but often cause intolerable side effects. Moclobemide is a well-tolerated alternative antidepressant, but there is a need for prospective controlled trials to evaluate its long-term efficacy.

Antidepressive Agents↗
PubMedDate not supplied

[Change in the catalytic properties of mitochondrial monoamine oxidase in experimental audiogenic epilepsy].

Catalytic properties of mitochondrial monoamine oxidases (MAO) were studied in brain, heart, liver and kidney of rats of Krushinskii-Molodkina strain with inherited audiogenic epilepsia. In brain of these rats a. 2.5-fold decrease of Vmax of serotonin (MAO-A substrate) deamination has been found. During audiogenic epileptiformic attack 2.5-5-fold decrease of Vmax of serotonin deamination in brain and liver and also decrease of benzylamine (MAO-B substrate) oxidation in brain were found. Simultaneously oxidation of glucosamine and gamma-aminobutyric acid was markedly increased (up to 5-fold and more) in brain. The data obtained showed that qualitative transformation occurred in catalytic properties of MAO which may be an important pathogenic factor in the development of epileptiformic attack.

Animals↗
PubMed1987

Tyramine pressor response with moclobemide--a reversible monoamine oxidase inhibitor.

Moclobemide is a reversible, short-acting monoamine oxidase inhibitor (MAO1), specific for MAO A. To study moclobemide effects on the tyramine pressor response, we gave 12 depressed patients (2 males, 10 females; mean age 47, SD 11 years) an i.v. tyramine test after 7 days drug free. The mean (+/- SD) tyramine dose to raise systolic blood pressure 30 mmHg was 5.6 +/- 2.5 mg. Repeat tyramine testing after 2 weeks of treatment with moclobemide (280 +/- 90 mg/d) showed the tyramine dose required was reduced to 2.5 +/- 1.6 mg (n = 8). The mean (+/- SD) increase in sensitivity to tyramine was 2.9 +/- 1.8. Four patients did not have repeated tyramine tests as testing was discontinued because of tyramine-induced cardiac arrhythmias. Moclobemide seems an effective antidepressant with less tyramine sensitivity than MAOIs in current use.

Adult↗
PubMed2006

New bioluminogenic substrates for monoamine oxidase assays.

Novel bioluminogenic substrates were designed for probing monoamine oxidase (MAO) activity based on a simple and effective beta-elimination strategy. By modifying the amino group and the central core of luciferin derivatives, we have developed a series of substrates useful for assays of MAO A or B, or both. One of these substrates, exhibiting low Km values and high signal-to-background ratios with both isozymes, was shown to accurately measure the Ki values of known MAO inhibitors. This substrate is a key component in the development of a highly sensitive homogeneous MAO assay for high-throughput screening (HTS) of compounds in drug discovery and for monitoring MAO activity in complex biological systems. This design strategy should be applicable to fluorogenic MAO substrates and could broaden the structural requirements of substrates for other enzyme assays.

Firefly Luciferin↗
PubMed1976

Metabolism of phenylethylamine in rat isolated perfused lung: evidence for monoamine oxidase 'type B' in lung.

Phenylethylamine is inactivated in a single passage through rat lung tissue by a process of uptake and deamination by a monoamine oxidase 'type B'. This enzyme is particularly susceptible to inhibition by deprenil and less sensitive to clorgyline. The monoamine oxidase of the lung, like that of other rat tissues, can be differentiated into 'type A' and 'type B' which appear to operate independently in the organized tissue.

Animals↗
PubMedDate not supplied

Monoamine oxidase inhibitor update. Potential adverse food and drug interactions.

Monoamine oxidase inhibitors (MAOIs) are medicines with potential for therapeutic gains, but they may also have adverse consequences. The risk: benefit ratio is assessed and, in appropriately selected cases, efficacy should outweigh disadvantages. Hypotension is the most prominent side-effect; yet the primary concern in the MAOI-treated person is to prevent co-exposure to substances with indirectly-acting sympathomimetic properties. Such co-utilisations from certain foods or drugs can result in dangerous hypertensive and hyperpyretic crises. A responsible individual should be involved in the administration of these drugs. The patient and family must fully understand the self-discretionary diet avoidance rules, which stress abstinence from high-tyramine foods. Drug prohibitions also emphasise elimination of indirect action sympathomimetics, but all pharmaceutical applications are always strictly controlled by the well informed physician who prescribes MAOIs. Treatment of the hypertensive crisis is urgent and includes alpha-blockade. Overdoses require supportive therapies and may necessitate acidification of the urine.

Drug Interactions↗
PubMed1983

Influence of hemodialysis on monoamine oxidase kinetics in platelets from chronic schizophrenic patients.

Platelet monoamine oxidase (MAO) activity in seven chronic schizophrenic patients undergoing hemodialysis treatment was studied. The treatment was performed in a double-blind crossover design. A significant increase in MAO activity was observed after 5 h of active dialysis, whereas inactive dialysis did not significantly alter the enzyme activity. The increase in MAO activity could be explained by the observed significant decrease in apparent Km values for the amine (phenethylamine) studied. During a treatment period of 8 weeks, the MAO activity was not significantly altered with either active or sham dialysis. No relation between clinical ratings and platelet MAO activity was observed. Plasma from the seven patients was collected before and after 5 h of active or inactive dialysis and incubated with rat brain mitochondrial MAO (RBM-MAO). No difference was noted in the RBM-MAO-activity-regulating properties of the plasma sampled during either sham or active dialysis.

Adult↗