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PubMed1986

Assignment of genes for human monoamine oxidases A and B to the X chromosome.

Monoclonal antibodies that immunoprecipitate human monoamine oxidase (MAO) A or human MAO B, but not the corresponding mouse enzymes, were used to assay for the presence of immunoprecipitable MAO A or MAO B (presumably coded by the respective human genes) in mouse-human hybrid somatic cell lines containing small numbers of human chromosomes. The results were as follow: Extracts of a human lymphoblastoid x mouse hepatoma hybrid line that retained the human X chromosome contained immunoprecipitable MAO B, while a similar hybrid line that contained the same human chromosomes, except for the human X, did not. Extracts of a human fibroblast x mouse neuroblastoma hybrid cell line, whose human chromosomal material consisted solely of the X, contained both immunoprecipitable MAO A and MAO B. Extracts of a related hybrid line, whose human chromosomal material consisted solely of an autonomous fragment and a fragment translocated to a mouse chromosome, contained immunoprecipitable MAO A. However, the level of immunoprecipitable MAO B activity in extracts of this hybrid was low or undetectable. Among extracts of 33 human fibroblast x mouse hepatoma hybrids that had been selected for expression of the X-linked human enzyme HPRT, 60% contained immunoprecipitable MAO B. This figure was comparable to the 58% that expressed the X-linked human isozyme for glucose-6-phosphate dehydrogenase (G6PD). When 11 of these hybrid lines, which contained immunoprecipitable MAO B and human HPRT, were selected for loss of HPRT, all lost immunoprecipitable MAO B in addition to HPRT. These data demonstrate that genes controlling the expression of MAO A and MAO B, which can be immunoprecipitated with the human-specific monoclonal antibodies, are located on the human X chromosome. Properties of the immunological epitopes recognized by the monoclonal antibodies suggest that the X-linked genes detected in this study are probably structural genes for the enzymes.

Chemical Precipitation↗
PubMedDate not supplied

[Effect of a new antiparkinsonian drug himantane on monoamine oxidase activity].

N-2(adamantyl)hexamethyleneimine hydrochloride (hemantane) is a new potential antiparkinsonian drug targeted at several neurochemical systems. The drug exhibits the properties of a low-affinity noncompetitive blocker of the ion channels of glutamate NMDA receptors. Hemantane increases the content of dopamine in the striatum, while decreasing the level of dopamine metabolite dioxyphenylacetic acid (DOPAC). Investigation of the drug interaction with monoamine oxidases (MAOs) of the A and B types in vitro showed that hemantane acts as a weak competitive inhibitor of MAO-B (Ki = 470 +/- 70 microM) and partly protected MAO-B from irreversible inhibition by selegiline (deprenyl), while virtually not influencing the activity of MAO-A. Administered to C57BL6 mice (20-100 mg/kg), hemantane did not influence the activity of MAO-B measured in isolated cerebral mitochondria. At the same time, hemantane administered in combination with deprenyl significantly reduced activity of the latter drug and caused pronounced irreversible inhibition of mitochondrial MAO-B (comparable with the effect of deprenyl introduced alone). Therefore, inhibition of MAO-B may contribute to the spectrum of neurochemical activity of hemantane.

Adamantane↗
PubMed2005

Evidence for reduced arterial plasma input, prolonged lung retention and reduced lung monoamine oxidase in smokers.

UNLABELLED: We have previously found that smokers have reduced brain monoamine oxidase (MAO) A and B using positron emission tomography (PET) and the irreversible mechanism-based radiotracers [(11)C]-labeled clorgyline (CLG) and deprenyl (DEP) and their deuterated analogs (D CLG, D DEP). More recently, we have estimated MAO A and B activity in other organs using the deuterium isotope effect to determine binding specificity for MAO and a three-compartment model to estimate k(3), the model term proportional to MAO A activity. Here, we have investigated the robustness of the model term k(3) for estimating lung MAO A and B in light of our unexpected finding that lung MAO activity (k(3)) was reduced for smokers relative to nonsmokers, although radiotracer uptake in the lungs was similar at peak and plateau for the two groups. METHODS: Time-activity data from lung and arterial plasma were used from seven nonsmokers and seven smokers scanned previously with CLG and D CLG, and five nonsmokers and nine smokers scanned previously with DEP and D DEP. The measured time-activity curves for lung and plasma and the integrals for the arterial plasma time-activity curves were compared at an early time point (2.5 min) and at the end of the study (55 min). A three-compartment irreversible model was used to estimate the differences between smokers and nonsmokers, and the stability of the parameter (k(3)) while varying model assumptions for the relative fractions of lung tissue, blood and air in the PET voxel. RESULTS: The peak in the arterial plasma input function and the integral of the arterial plasma time-activity curve over the first 2.5 min after radiotracer injection were significantly lower for smokers relative to nonsmokers for all four tracers. However, although the peak and plateau of the lung time-activity curves were similar for smokers and nonsmokers, the decline in radioactivity from peak to plateau was slower for smokers for all tracers. Using a three-compartment irreversible model, we estimated the ratio of MAO subtypes A and B in normal lung tissue to be on the order of 3 to 1 (MAO A to B) and that smokers have reduced MAO levels for both subtypes as measured by the model parameter, k(3). The values of k(3) are insensitive to model assumptions of variations in air and tissue fraction in the PET voxel. Most of the effects of changes in these fractions are absorbed into the parameter K(1), which governs the plasma-to-tissue transfer of tracer and is a function of blood flow. K(1) was found to be larger in smokers, although the values depend upon model assumptions of air and tissue fractions. k(3) was found to be significantly lower in smokers; for CLG, a 50% reduction in MAO A for both CLG and D CLG was observed. For DEP, k(3) was also significantly lower in smokers with a reduction of approximately 80% in lung MAO B, although there was a very large coefficient of variation in the smoker's k(3). We also found larger values of lambda (K(1)/k(2)) for smokers relative to nonsmokers for all tracers consistent with a longer lung retention of the nonenzyme-bound tracer, which explains the slower decline in uptake from peak radioactivity for smokers. CONCLUSIONS: The measured arterial input function values for smokers and nonsmokers are significantly different for these two tracer pairs for nonsmokers and smokers particularly for the first few minutes after radiotracer injection. Model estimates of k(3) that indicate that smokers have lower lung MAO A and B activity than nonsmokers are robust and insensitive to variations in model assumptions for relative fractions of lung tissue, blood and air in the PET voxel. Although we have only investigated the behavior of [(11)C]clorgyline and [(11)C]l-deprenyl and their deuterium-substituted analogs in this report, the extent to which reduced arterial input and longer lung retention also hold for other tracers for subjects who smoke merits investigation.

Arteries↗
PubMed2003

Inhibition of monoamine oxidase B by selective adenosine A2A receptor antagonists.

Adenosine receptor antagonists that are selective for the A(2A) receptor subtype (A(2A) antagonists) are under investigation as possible therapeutic agents for the symptomatic treatment of the motor deficits associated with Parkinson's disease (PD). Results of recent studies in the MPTP mouse model of PD suggest that A(2A) antagonists may possess neuroprotective properties. Since monoamine oxidase B (MAO-B) inhibitors also enhance motor function and reduce MPTP neurotoxicity, we have examined the MAO-B inhibiting properties of several A(2A) antagonists and structurally related compounds in an effort to determine if inhibition of MAO-B may contribute to the observed neuroprotection. The results of these studies have established that all of the (E)-8-styrylxanthinyl derived A(2A) antagonists examined display significant MAO-B inhibitory properties in vitro with K(i) values in the low micro M to nM range. Included in this series is (E)-1,3-diethyl-8-(3,4-dimethoxystyryl)-7-methylxanthine (KW-6002), a potent A(2A) antagonist and neuroprotective agent that is in clinical trials. The results of these studies suggest that MAO-B inhibition may contribute to the neuroprotective potential of A(2A) receptor antagonists such as KW-6002 and open the possibility of designing dual targeting drugs that may have enhanced therapeutic potential in the treatment of PD.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1995

Rat brain monoamine oxidase A and B inhibitory (tribulin) activity during drug withdrawal anxiety.

Morphine (10 mg/kg), ethanol (8% w/v, 2 ml/kg), nicotine (0.1 mg/kg), cannabis extract (200 mg/kg), lorazepam (10 mg/kg) and ondansetron (0.1 mg/kg) were each administered to rats twice daily i.p. for 14 days and the anxiogenic response following their withdrawal was monitored by the elevated plus-maze test 24 h later. Brains were removed and endogenous monoamine oxidase (MAO) A and B inhibitory activity (tribulin) levels measured on day 14 and 24 h after drug withdrawal in different groups of animals. Morphine, ethanol, lorazepam and nicotine withdrawal was associated with significant anxiety and corresponding increase in brain tribulin activity, particularly its MAO A inhibitory component. Cannabis and ondansetron withdrawal were neither associated with anxiety or change in tribulin levels. The investigation supports the postulated role of tribulin as an endogenous correlate of anxiety, its MAO A inhibitory component accounting for a major part of this effect.

Animals↗
PubMed2004

Monoamine oxidase inhibition and CNS immunodeficiency infection.

HIV invades CNS subcortical areas, particularly the dopamine-rich basal ganglia and induces a subcortical dementia. Data suggest that the basal ganglia dysfunction plays a critical role in the neuropsychiatric manifestation of HIV infection. Therefore, therapeutic approaches for HIV dementia nowadays wish to include apart from the highly active antiretroviral therapy (HAART) also adjunctive medication. In this short article, we report briefly on neurotoxicity associated with the immunodeficiency virus and discuss the effects of selegiline, a monoamine oxidase inhibitor which enhances dopamine availability in CNS on immunodeficiency virus-induced neurological disease.

Animals↗
PubMed2002

Effect of TV3326, a novel monoamine-oxidase cholinesterase inhibitor, in rat models of anxiety and depression.

RATIONALE: A high incidence of depression is found in subjects with Alzheimer's disease (AD), in whom many antidepressants are contraindicated because they have anticholinergic activity. We have designed a new cholinesterase inhibitor TV3326 [( N-propargyl-(3R) aminoindan-5-yl)-ethyl methyl carbamate] for the treatment of AD, which has neuroprotective activities and also blocks monoamine oxidase (MAO) A and B in the brain but not in the intestine after chronic administration. OBJECTIVES: To examine the antidepressant and anxiolytic potential of TV3326 in rats and compare them with those of its R isomer TV3279, which lacks MAO-inhibitory activity, and of amitriptyline and moclobemide. METHODS: Each of the drugs was administered orally, acutely or once daily for 2 weeks, and its effect was evaluated on the behavior of rats in the forced swim test (FST) and plus maze (EPM) test. RESULTS: Immobility in the FST was reduced by 56% after acute and chronic administration of amitriptyline (10 mg/kg) and by 42% after acute administration of moclobemide (20 mg/kg) and by 63% when this drug was given chronically. TV3326 (26 mg/kg) only reduced immobility (by 44%) when given chronically and inhibited brain MAO-A and -B by more than 66%. TV3279 had no significant effect in the FST. All the drugs except TV3326 increased anxiogenic activity in rats in EPM, as indicated by a more than 50% decrease in the time in open arms after chronic administration. CONCLUSIONS: TV3326 has potential antidepressant-like activity when given in a dose regimen that causes significant inhibition of brain MAO-A and -B. Together with its neuroprotective properties, this action could make TV3326 a potentially valuable drug for the treatment of dementia in patients with depression.

Animals↗
PubMed2004

Cardiovascular activity of rasagiline, a selective and potent inhibitor of mitochondrial monoamine oxidase B: comparison with selegiline.

Selegiline is used for treating Parkinson's disease. Despite its efficacy, the clinical use of selegiline in combination with l-dihydroxphenylalanine in Parkinsonian patients is hampered by cardiovascular complications, such as hypotension. This study was designed to compare in rats the cardiovascular effects of selegiline and rasagiline, their metabolites l-methamphetamine and aminoindan (TVP-136), respectively, and the second rasagiline metabolite non-monoamine oxidase (MAO) inhibitor TVP-1022 (N-propargyl-1S(-)aminoindan). Intravenous (i.v.) administration of selegiline and rasagiline (1 mg kg(-1)) to anaesthetized rats (thiobutabarbital, 100 mg kg(-1), i.p.) did not affect mean arterial pressure (MAP), carotid blood flow (CBF) or carotid vascular resistance (CVR). Selegiline (10 mg kg(-1), i.v.) decreased MAP, CBF and increased CVR. In contrast, rasagiline (10 mg kg(-1), i.v.) caused a small transient decrease in MAP, while CBF and CVR were unchanged. l-methamphetamine (1 mg kg(-1), i.v.) administration provoked a dramatic and long-lasting depressor response, decreased CBF and increased CVR. In contrast, injection of aminoindan or TVP-1022 at a similar dose produced gradual nonsignificant decreases in MAP and CBF. Chronic oral treatment (21 days) of awake rats with selegiline at 10 mg kg(-1) decreased systolic blood pressure (SBP), diastolic blood pressure (DBP), and MAP, whereas heart rate was unaffected. Since the effective MAO-B inhibitory and clinical dose of rasagiline is about one-tenth that of selegiline, administration of 1 mg kg(-1) day(-1) rasagiline resulted in moderate decreases in SBP, DBP, and MAP, which were significantly lower than those caused by the 10 mg kg(-1) day(-1) dose of selegiline. These findings indicate that rasagiline, when given at doses equivalent to selegiline, is less likely to be hypotensive.

Administration, Oral↗
PubMed1994

Different metabolism of norepinephrine and epinephrine by catechol-O-methyltransferase and monoamine oxidase in rats.

Normetanephrine (NMN) and metanephrine (MN), are the O-methylated metabolites of norepinephrine (NE) and epinephrine (E), whereas dihydroxyphenylglycol (DHPG) is the deaminated metabolite of both NE and E. This study compared production of NMN, MN and DHPG during tracer and high-dose infusions of Ne and E in rats, with and without inhibition of catechol-O-methyltransferase (COMT) or the A and B forms of monoamine oxidase (MAO). Animals also received infusions of NMN and MN to compare plasma clearances and spillovers of NMN and MN with and without MAO inhibition. Inhibition of COMT increased plasma DHPG and decreased plasma NMN and MN, whereas inhibition of MAO decreased plasma DHPG and increased plasma NMN and MN. The increase in NMN and MN after MAO inhibition reflected blocked deamination of NMN and MN by MAO-A, but not MAO-B. The A form of MAO was also largely responsible for deamination of NE. Infused E was deaminated to DHPG less efficiently than NE. High doses of infused E were O-methylated more efficiently than NE, whereas tracer doses were O-methylated similarly. After MAO inhibition NE was O-methylated more efficiently than E. Increased plasma NMN after MAO inhibition reflected the combined effects of a decrease in the plasma clearance of NMN and an increase in the spillover of NMN into plasma, whereas the smaller increase in plasma MN was due solely to a decrease in the plasma clearance of MN. Thus, E and MN are not deaminated at extraneuronal sites of O-methylation, whereas NE is both O-methylated and deaminated with proportionally more deaminated than O-methylated as the concentration of NE increases. The above results support the preference of NE over E for neuronal pathways of metabolism, but indicate considerably more complex differences in the metabolism of NE and E by extraneuronal O-methylation and deamination.

Animals↗
PubMed2006

(-)-Trans-epsilon-viniferin, a polyphenol present in wines, is an inhibitor of noradrenaline and 5-hydroxytryptamine uptake and of monoamine oxidase activity.

(-)-Trans-epsilon-viniferin (epsilon-viniferin, 5-200 microM), a dimer of resveratrol, concentration-dependently inhibited the uptake of [3H]noradrenaline and [3H]5-HT by synaptosomes from rat brain (being slightly but significantly more selective against [3H]noradrenaline) and the uptake of [3H]5-HT by human platelets. On the other hand, epsilon-viniferin (5-200 microM) concentration-dependently inhibited the enzymatic activity of commercial (human recombinant) monoamine oxidase (MAO) isoform (MAO-A and MAO-B) activity, being slightly but significantly more selective against MAO-B than against MAO-A. Taking into account that the principal groups of drugs used to treat major depression are noradrenaline/5-HT uptake or MAO inhibitors, under the assumption that epsilon-viniferin exhibits a similar behaviour in humans in vivo, our results suggest that this natural polyphenol may be of value as a structural template for the design and development of new antidepressant drugs with two important biochemical activities combined in the same chemical structure: noradrenaline/5-HT uptake and MAO inhibitory activity.

Animals↗
PubMed1990

The effects of soman in vitro on catechol-O-methyltransferase and monoamine oxidase activities in rabbit tissues.

Soman (pinacolyl methylphosphonofluoridate) not only increases acetylcholine levels by inhibiting cholinesterases, it also alters the levels of some other neurotransmitters including norepinephrine, dopamine, and serotonin. Soman also causes an alteration in the activities of the enzymes metabolizing norepinephrine when it is administered to animals. Because these alterations may result from indirect effects on the enzymes, the effects of in vitro application of soman on catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) activities in rabbit tissues were investigated. Enzyme activities were determined in rabbit lung, liver, cerebellum, cerebrum, brain stem, mesenteric artery, pulmonary artery, renal artery, central ear artery, thoracic aorta, and diaphragm. MAO and COMT activities were not affected by soman in any tissues tested, except the lung and liver, where the activity of COMT was increased (p less than 0.05). Thus, reported effects of soman in vivo on norepinephrine, dopamine, or serotonin concentrations, and MAO and COMT activities do not seem to result from direct effects on the activities of these amine-metabolizing enzymes.

Animals↗
PubMed1984

Oxidation of the neurotoxic amine 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) by monoamine oxidases A and B and suicide inactivation of the enzymes by MPTP.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a thermal breakdown product of a meperidine-like narcotic analgetic used by drug abusers as a synthetic heroin, causes Parkinsonian symptoms in humans and degeneration of the substantia nigra in monkeys. MPTP is oxidized by brain mitochondrial preparations in a process which is blocked by deprenyl and pargyline, implying catalysis by monoamine oxidase B. The present paper demonstrates that pure MAO B isolated from beef liver oxidizes MPTP 38% as fast as benzylamine with a comparable Km value. Additionally, MAO A, isolated from human placenta, oxidizes MPTP to the same product at about 12% of the rate of kynuramine, again with a comparable Km value. The latter reaction is blocked by clorgyline. Both forms of MAO are progressively inactivated by MPTP by a process which follows first order kinetics. This progressive inactivation and the fact that the activity of MAO B is not significantly regenerated following gel exclusion chromatography suggest the formation of a covalent adduct with enzyme. Thus, MPTP appears to be a suicide inactivator of MAO.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1988

[Monoamine oxidase inhibition by pyrrole quinoline derivatives].

The effect of 1-(beta-aminoethyl)-3H-pyrrole[2,3-h]quinoline (I), 3-(beta-aminoethyl)-1H-pyrrole[2,3-h]quinoline (I'), 8-amino-3H-pyrrole[2,3-h]quinoline (II), 6-amino-3H-pyrrole[2,3-h]quinoline (II') and 8-amino-1H-pyrrole[2,3-h]quinoline (III) on tyramine, serotonin and 2-phenylethylamine deaminase activities of mitochondrial monoamine oxidase from bovine brain were studied. All the compounds tested appeared to be reversibly inhibit MAO without preliminary incubation. Compounds II, II' and III specifically inhibited type A MAO; compound III exhibited the highest selectivity. The inhibition was of a mixed type. The effects of compounds I and I' were competitive and inconsistent with a classical concept on the dual activity of MAO, i. e., deamination of tyramine, a substrate common for MAO type A and MAO type B was inhibited in a greater degree than the deamination of specific substrates of MAO type A (serotonin) or type B (2-phenylethylamine). Possible reasons for the observed phenomenon are discussed.

Animals↗
PubMed1995

Changes in platelet monoamine oxidase and plasma dopamine-beta-hydroxylase activities in lithium-treated bipolar patients.

The activity of monoamine oxidase (MAO) and dopamine-beta-hydroxylase (DBH), enzymes involved in monoamine metabolism, were studied in 29 bipolar patients (mean age = 33.12 years, SD = 7.27) who were treated with lithium carbonate and in 20 healthy volunteers (mean age = 30.05 years, SD = 6.04). Platelet MAO activity was higher after lithium withdrawal, whereas plasma DBH activity was lower in remitted euthymic bipolar patients compared with normal volunteers. During lithium treatment, platelet MAO activity decreased and plasma DBH activity increased compared with the lithium-withdrawal values. It was also observed that the activities of these enzymes in the bipolar patients during lithium treatment did not differ from those in the volunteers. Thus, platelet MAO and plasma DBH activities differed in unmedicated patients with bipolar affective disorder from those of healthy subjects. Treatment with lithium appeared to have a normalizing effect on MAO and DBH activity levels.

Adult↗
PubMed2002

Kinetic interactions of dopamine and dobutamine with human catechol-O-methyltransferase and monoamine oxidase in vitro.

Dopamine and dobutamine are often infused together into acutely ill patients requiring temporary support of cardiac and renal function, but whether these catecholamines affect the metabolic clearance of each other is not established. We determined the kinetics of dopamine and dobutamine as substrates and inhibitors of each other, i.e., apparent V(max), K(m), and K(i), with crude preparations of human blood mononuclear cell catechol-O-methyltransferase (COMT) and platelet monoamine oxidase (MAO) at pH 7.4 and 37 degrees C. Values of V(max) for dopamine and dobutamine as substrates for COMT were 0.45 and 0.59 nmol of 3-O-methyl product formed per milligram of protein per minute, whereas those for K(m) were 0.44 and 0.05 mM, respectively. Dopamine and dobutamine were competitive inhibitors of each other in this reaction. The K(i) for dopamine as an inhibitor of dobutamine methylation was 1.5 mM, whereas that for dobutamine as an inhibitor of dopamine methylation was 0.015 mM. Dopamine but not dobutamine was a substrate for MAO. The V(max) for dihydroxyphenylacetaldehyde formation from dopamine was 0.29 nmol/mg protein/min and the K(m) for dopamine was 0.38 mM. Dobutamine was a noncompetitive inhibitor of dopamine oxidation in this reaction (K(i) congruent with 1.19 mM). The high apparent K(m) and K(i) values derived for dopamine and dobutamine when tested with these two human enzymes in vitro suggest that these catecholamines do not interfere with the metabolism of each other when both are infused together at therapeutic concentrations.

Adult↗
PubMed1984

Monoamine oxidase inhibitors in South American hallucinogenic plants: tryptamine and beta-carboline constituents of ayahuasca.

Ayahuasca is a hallucinogenic beverage derived by boiling the bark of the Malpighiaceous liana Banisteriopsis caapi together with the leaves of various admixture plants, viz. Psychotria viridis, Psychotria carthagenensis , or Diplopterys cabrerana . B. caapi contains harmine, harmaline, and tetrahydroharmine while the admixtures contain N,N-dimethyltryptamine (DMT). DMT, a potent hallucinogen, is inactive orally due to degradation by visceral monoamine oxidase (MAO). The beta-carbolines, however, are highly active reversible inhibitors of MAO and may protect the DMT from deamination by MAO and render it orally active. This mechanism has been proposed to underlie the oral activity of ayahuasca but has not been experimentally confirmed. In the present study the constituents of the admixture plants and the alkaloids of eight ayahuasca samples from Peru were qualitatively and quantitatively analyzed using two-dimensional thin-layer chromatography (TLC), high pressure liquid chromatography (HPLC) and gas chromatography/mass spectrometry (GC/MS). Several B. caapi cultivars were quantitatively compared for variations in alkaloid content. Three admixture plants used rarely in the manufacture of ayahuasca were also screened for alkaloids. A selected sample of beta-carbolines were screened for activity as MAO inhibitors using an in vitro assay system, and structure/activity relationships were compared. Inhibition observed with single compounds was compared with the activity of selected samples of ayahuasca which were screened in the system and also with the activity of mixtures of beta-carbolines. The levels of DMT and beta-carbolines found in the ayahuasca samples examined in the present study were an order of magnitude greater than the levels reported in a previous study. Ayahuasca was found to be an extremely effective inhibitor of MAO in vitro and the degree of inhibition was directly correlated with the concentration of MAO-inhibiting beta-carbolines. Inhibition experiments using mixtures of beta-carbolines indicated that their effects in combination are additive, rather than synergistic or antagonistic. Implications of the results in understanding the pharmacology of ayahuasca are discussed.

Alkaloids↗