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PubMedDate not supplied

Age-related increases in brain monoamine oxidase B in living healthy human subjects.

Several studies of human brain postmortem report that monoamine oxidase B (MAO B) increases with age and it has been proposed that this increase reflects age-associated increases in glial cells. We measured brain MAO B in a group of normal healthy human subjects (n = 21; age range 23-86; 9 females and 12 males; nonsmokers) using [11C]L-deprenyl-D2 and positron emission tomography. Brain glucose metabolism was also measured with 18FDG in 15 of the subjects. MAO B increased (p < 0.004) in all brain regions examined except the cingulate gyrus. In contrast, subjects showed the expected regional age-related decreases in blood flow and metabolism. In the 15 subjects in whom both MAO B and LCMRglu was measured, there was a trend (p < 0.03) toward an inverse association between brain glucose metabolism and MAO B activity in the frontal and parietal cortices. Although the age-related increase in brain MAO B in living subjects is consistent with postmortem reports, the degree of increase is generally lower.

Adult↗
PubMedDate not supplied

[Derivatives of 4-phenylpiperidine as substrates of rat brain monoamine oxidase].

A rate of utilization of 4-phenyl piperidine and its 12 derivatives by brain monoamine oxidase (MAO) was studied as compared with typical neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The enzyme was isolated from P2 synaptosomal fraction of brain corpus striatum of Sprague-Dawley rats. 10 drugs were oxidized in the MAO-catalyzed reaction with the rate close or similar to the MPTP oxidation while 6 of them exhibited the neurotoxic effect. Analysis of MAO inhibition, using 1 microM of chlorgyline and/or deprenyl, enabled to evaluate the contribution of MAO-A and MAO-B forms to utilization of 1 mM content of the substances studied. MAO-B was shown to oxidize preferably the drugs radicals of which were substituted at 3rd position of the piperidine ring, while MAO-A preferred the derivatives with radical substitution at 4th position. The rate of substrate oxidation was decreased distinctly after introduction of complete substituents into the 3rd and 4th positions of the nitrogenous heterocycle; at the same time, presence of cyclic fluorine-containing structures increased the rate of utilization, similar to that of MPTP oxidation. Derivatives of 4-phenyl piperidine, which contained in a number of drugs, were oxidized in the MAO-catalyzed reactions and might exhibit direct- or side-neurotoxic effects.

Animals↗
PubMed1986

Inhibition of monoamine oxidase in monoaminergic neurones in the rat brain by irreversible inhibitors.

The irreversible inhibition of monoamine oxidase (MAO) inside and outside monoaminergic neurones in the rat brain by the suicide inhibitors clorgyline, selegiline (l-deprenyl), pheniprazine, phenelzine, iproniazid, pargyline and the d- and l-enantiomers of tranylcypromine was determined. This was achieved by incubating crude synaptosomal preparations of hypothalamus and striatum from rats treated with the inhibitors 24 hr earlier, with low concentrations of [14C]serotonin (0.1 microM), [14C]-noradrenaline (0.25 microM) and [14C]dopamine (0.25 microM) in the absence and presence of selective uptake inhibitors (citalopram, maprotiline and amfonelic acid, respectively). It was found that all inhibitors inhibited the deamination of serotonin and noradrenaline outside the amine neurons at slightly lower doses than that within these neurones. This could at least in part be due to protection of MAO by the endogenous amines in these neurones. The deamination of dopamine was rather more strongly inhibited inside the neutrons than outside, particularly at higher doses. There was no indication that tranylcypromine or phenelzine was accumulated in the neurones by the membranous amine uptake mechanisms. The rate of the recovery of the deaminating activities inside and outside the serotonergic and noradrenergic neurones in hypothalamus after phenelzine and clorgyline inhibition was the same (50% recovery after 12-15 days), which indicates similar rate of synthesis of MAO in different cell types.

Animals↗
PubMed2000

Association between a functional polymorphism in the monoamine oxidase A gene promoter and major depressive disorder.

Various polymorphisms of the X-chromosomal monoamine oxidase A (MAO-A) gene were investigated for association with affective disorders. However, none of the studied variants could consistently be associated with either major depressive or bipolar affective disorder. Recently, a positive association between panic disorder and a novel functional repeat polymorphism in the MAO-A gene promoter, with the longer alleles being more active, was reported. Since monoaminergic neurotransmission is supposed to play an important role in affective disorders, we investigated a potential association of this polymorphism with major depressive illness in a sample of 146 unrelated patients of German descent and a control group of 101 individuals with a negative life history for affective disorders. Similarly to the recent findings in panic disorder, we observed a significantly increased frequency of genotypes containing only long alleles in female patients with recurrent major depression in comparison with age- and sex-matched controls. Thus, our data suggest that an excess of high-activity MAO-A gene promoter alleles resulting in an elevated MAO-A activity is a risk factor for major depressive disorder in females. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:801-803, 2000.

Adult↗
PubMed1998

Evidence of a coupled mechanism between monoamine oxidase and peroxidase in the metabolism of tyramine by rat intestinal mitochondria.

The relationship between monoamine oxidase (EC 1.4.3.4; MAO) and peroxidase (EC 1.11.1.7; POD) in the metabolism of tyramine was investigated using the crude mitochondrial fraction of rat intestine. When tyramine was incubated with mitochondria, the formation of the peroxidase-catalysed oxidation product, 2,2'-dihydroxy-5,5'-bis(ethylamino)diphenyl (dityramine), identified by mass spectrometric analysis, was monitored spectrophotometrically. After an initial lag time, the formation rate of dityramine was linear up to 2 hr, amounting to 17 nmol x hr(-1) x mg protein(-1). A similar value was found for the oxidative deamination of tyramine catalysed by intestinal MAO. Either 10(-3) M clorgyline or 10(-3) M NaCN suppressed this reaction by completely inhibiting MAO or POD, respectively. In the former case, however, addition of H2O2 to the incubation mixture promptly started the reaction. Selective inhibition of MAO-A and MAO-B was achieved with 3 x 10(-7) M clorgyline and 3 x 10(-7) M deprenyl, respectively, and the formation rate of dityramine decreased in a corresponding manner. Preincubation with histamine or spermidine reduced the lag time without affecting the steady-state reaction rate. Higher levels of dityramine were also detected in vivo in rat intestine after oral administration of tyramine. These results indicate that the peroxidase-dependent metabolism of tyramine in the gut may be driven by H2O2 produced by MAO activities and that MAO-A is mainly responsible for this process, as well as for the oxidative deamination of tyramine.

Animals↗
PubMed1997

Monoamine oxidase inhibitory properties of some methoxylated and alkylthio amphetamine derivatives: structure-activity relationships.

The monoamine oxidase (MAO) inhibitory properties of a series of amphetamine derivatives with different substituents at or around the para position of the aromatic ring were evaluated. In in vitro studies in which a crude rat brain mitochondrial suspension was used as the source of MAO, several compounds showed a strong (IC50 in the submicromolar range), selective, reversible, time-independent, and concentration-related inhibition of MAO-A. After i.p. injection, the compounds induced an increase of serotonin and a decrease of 5-hydroxyindoleacetic acid in the raphe nuclei and hippocampus, confirming the in vitro results. The analysis of structure-activity relationships indicates that: molecules with amphetamine-like structure and different substitutions on the aromatic ring are potentially MAO-A inhibitors; substituents at different positions of the aromatic ring modify the potency but have little influence on the selectivity; substituents at the para position such as amino, alkoxyl, halogens, or alkylthio produce a significant increase in the activity; the para-substituent must be an electron donor; bulky groups next to the para substituent lead to a decrease in the activity; substituents located at positions more distant on the aromatic ring have less influence and, even when the substituent is a halogen (Cl, Br), an increase in the activity of the compound is obtained. Finally, the MAO-A inhibitory properties of some of the compounds evaluated are discussed in relation to: (a) potential antidepressant activity, and (b) their reported hallucinogenic, neurotoxic, or anxiolytic effects.

Amphetamines↗
PubMed2006

Adaptive and maladaptive impulsivity, platelet monoamine oxidase (MAO) activity and risk-admitting in different types of risky drivers.

RATIONALE: Platelet monoamine oxidase (MAO) activity reflects serotonergic functioning associated with impulsive behaviour, but the significance of these associations to real-life impulsive behaviour in healthy subjects is not clear. OBJECTIVES: The present study explores impulsivity and platelet MAO activity among people with driving violations. MATERIALS AND METHODS: We compared facets of impulsivity and platelet MAO activity in 1,004 male drivers, out of whom 203 had been caught by the police driving drunk and 292 had been caught exceeding speed limits and committing other non-alcohol-related driving violations. Subjects with speeding and other non-alcohol-related violations were further divided according to their self-reported risk-admitting of exceeding speed limits. RESULTS: While drunk driving was associated only with maladaptive types of impulsivity, exceeding speed limits was associated with functional impulsivity and excitement seeking and, to a lesser degree, with dysfunctional impulsivity. Drunk drivers had lower platelet MAO activity. Risk-admitting high-risk drivers had higher platelet MAO activity, neuroticism-related impulsivity, dysfunctional impulsivity and excitement seeking compared to all other groups and higher functional impulsivity compared to controls. Risk-denying high-risk drivers had only higher functional impulsivity compared to controls. CONCLUSIONS: This study demonstrates different expressions of functional and dysfunctional impulsivity in behaviour. While platelet MAO activity is lower in alcohol-related risky behaviour, non-alcohol-related self-acknowledged risky behaviour is related to higher platelet MAO activity. Thus, deviance towards lower as well as higher end of central serotonergic functioning may lead to impulsive behaviour. While self-reported impulsivity did not correlate with MAO activity, both MAO activity and impulsivity were related to risky behaviour.

Adult↗
PubMed1997

Specific and amplified current responses to histidine and histamine using immobilized copper-monoamine oxidase membrane electrode, based on novel ascorbate oxidase activity induced by exogenous ligands.

Upon the addition of histidine and histamine, the copper containing monoamine oxidase (MAO) catalyzes the oxidation of L-ascorbic acid (AsA) by dissolved oxygen, in which the consumed oxygen was finally converted to hydrogen peroxide, according to Michaelis-Menten kinetics (Km) = 1.97 mM, upon the addition of 5 x 10(-5) M L-histidine at 35 degrees C and pH 8.5). The amount of oxygen consumption depended on the amount of histidine and histamine added, and specific responses over other amines were observed when the oxygen electrode modified with immobilized MAO membrane was used in the 0.1 M Tris buffer containing AsA. The calibration curves of L-histidine and histamine at 4 mM AsA exhibit linearity in the concentration range from 5 x 10(-7) to 5 x 10(-5) M L-histidine and 5 x 10(-6) to 1 x 10(-8) M histamine, with detection limit of 3 x 10(-7) M L-histidine and 3 x 10(-6) M histamine, respectively. The ESR signal of copper(II) in active site of MAO at 77K was apparently changed upon the addition of L-histidine and histamine indicating that exogenous histidine and histamine bound to the copper site of enzyme and lead to the structural change in active site.

Animals↗
PubMed1995

Monoamine oxidase inhibitors in posttraumatic stress disorder. Promise and problems in Indochinese survivors of trauma.

An examination of the available literature supports the efficacy of monoamine oxidase inhibitors (MAOIs) in treating posttraumatic stress disorder (PTSD). This effect may or may not be independent of the response of symptoms of major depression; there is suggestive but inconclusive evidence supporting both. Additionally, evidence is accumulating that the avoidance symptoms of PTSD respond less reliably to chemotherapy and may be less important in characterizing this entity than the intrusive recollection of traumatic events and hyperarousal symptoms; clinical cases from the Indochinese Psychiatry Clinic support this assertion. Concerns about the clinical use of MAOIs in the Indochinese population are raised, as is work in progress on reversible inhibitors of monoamine oxidase-A that may effectively address those concerns. A recent suggestion that PTSD may be one of a family of affective disorders is discussed in light of the treatment effects of MAOIs and clinical experience with Southeast Asian survivors of mass violence.

Adult↗
PubMed1975

Differential effects of inhibitors of monoamine oxidase Types A and B on the adrenergic system of the rabbit iris.

Topical instillation of inhibitors of monoamine oxidase Types A and B into the rabbit eye, followed by the administration of a releaser of monoamines (Ro 4-1284), induces strong and sustained dilation of the iris. The mydriatic pattern differs markedly with A- and B-inhibitors and with the duration of the inhibitor treatment. The Type B inhibitor, deprenyl, prevents the degradation of exogenous 2-phenylethylamine and possibly of the endogenous amine X capable of releasing monoamines from a compartment less accessible to Ro-1284.

5-Methoxytryptamine↗
PubMed1978

Pressor amines and monoamine-oxidase inhibitors for treatment of postural hypotension in autonomic failure. Limitations and hazards.

The short-term effects of pressor amines were investigated in four patients with postural hypotension caused by autonomic failure. In supine patients p-tyramine alone or with a monoamine-oxidase inhibitor produced pronounced supine hypertension without abolishing the symptoms associated with a postural fall in blood-pressure. Phenylephrine or ephedrine maintained a normal blood-pressure on standing but caused supine hypertension. Thus the effects of p-tyramine with or without a monoamine-oxidase inhibitor were unpredictable and did not include relief of postural hypotension. Phenylephrine or ephedrine had some beneficial effect, but since all these drugs influence standing pressure only at the expense of pronounced supine hypertension, alternative therapy must be sought.

Aged↗
PubMed1982

Inhibition of dimethylnitrosamine metabolism by some heterocyclic compounds and by substrates and inhibitors of monoamine oxidase in the rat.

Pretreatment of rats with a number of nitrogen-containing heterocyclic compounds was found to inhibit markedly the metabolism of dimethylnitrosamine (DMN) in terms of both CO2 excretion and decline in blood DMN concentration. However, many of these compounds had either much less or no inhibitory effect on the in vivo metabolism to CO2 of a typical mixed-function oxidase substrate, aminopyrine. In addition, a number of model inhibitors of monoamine oxidase (MAO) activity also inhibited DMN metabolism in the intact animal, and a number of primary amines, known substrates of hepatic MAO, inhibited DMN metabolism but not that of aminopyrine in the isolated perfused liver system. These results, together with in vitro data and previously reported studies on the effect of MAO inhibitors and substrates on the mutagenicity of DMN, suggest that the metabolism and bioactivation of DMN may be in part mediated by a MAO type of enzyme activity.

Aminopyrine↗