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PubMed2000

Evaluation of a ginkgo biloba extract (EGb 761) in functional tests for monoamine oxidase inhibition.

A standardized extract of ginkgo biloba (EGb 761) was evaluated in functional tests for monoamine oxidase (MAO) inhibition in mice: l-dihydroxyphenylalanine (CAS 59-92-7,1-DOPA) potentiation, tryptamine (CAS 61-54-1) potentiation, 5-hydroxytryptophan (CAS 4350-07-6,5-HTP) potentiation and phenylethylamine (CAS 64-04-0) potentiation. The doses investigated (25, 50 and 100 mg/kg p.o once daily for 5 days) were those known to possess anti-stress properties in other animal models. In contrast to the reference substances investigated (nialamide (CAS 51-12-7), clorgyline (CAS 17780-75-5) and 1-deprenyl (CAS 14611-52-01), EGb 761 did not exhibit any activity indicative of MAO inhibition. It was concluded that MAO inhibition was not the mechanism primarily responsible for EGb 761's anti-stress activity.

5-Hydroxytryptophan↗

PubMed1999

Histochemical study of dopamine-degrading monoamine oxidase activity in dopaminergic neurons of rat brain.

We examined whether dopamine-degrading activity of monoamine oxidase (MAO) is present in dopaminergic neurons of the rat brain. We employed a double-labeling procedure combining immunohistochemistry for tyrosine hydroxylase (TH) and enzyme histochemistry for MAO activity using dopamine as a substrate. The following dopaminergic cell groups were examined: A16 (glomerular layer of the olfactory bulb), A14 (hypothalamic periventricular region), A13 (zona incerta), A12 (arcuate nucleus), A11 (periventricular gray matter of the caudal thalamus), A10 (ventral tegmental area), A9 (substantia nigra pars compacta, SNC) and A8 (retrorubral nucleus). Although no MAO activity was detected in any of the TH-immunoreactive dopaminergic neurons, strong dopamine-degrading MAO activity was found in TH-positive neurons in the locus coeruleus (LC) (i.e., noradrenergic neurons). Our results indicate that dopamine-degrading MAO activity is very low in dopaminergic neurons compared to the MAO activity in LC noradrenergic neurons.

Animals↗

PubMed1982

Monoamine oxidase inhibitory modulators in rat heart cytosol: evidence for induction by thyroid hormone.

Inhibitory modulators of monoamine oxidase (MAO) were found in rat heart 105,000 X g supernatant. The modulators inhibited MAO activity present in the outer mitochondrial membrane. The inhibition was noncompetitive when using membrane-associated MAO as enzyme source. The modulators did not, however, inhibit the enzyme activity in the soluble fraction prepared from outer mitochondrial membranes. MAO inhibitory modulator concentration in rat heart cytosol was increased by the administration of T4 to rats. Three different inhibitory molecules were identified by gel filtration studies. These results suggest that thyroid hormone regulates membrane-associated MAO activity via the production of MAO inhibitory modulators, that the modulators probably bind to specific sites on the outer mitochondrial membrane, and that this binding of modulators to the membranes may result in a structural change in the mitochondrial membrane and a decrease in MAO enzyme activity.

Animals↗

PubMed1979

Histochemical detection of monoamine oxidase activity in smooth muscle and epithelial tissues of Mytilus edulis L. and Mytilus galloprovincialis Lmk.

Monoamine oxidase (MAO) activity was detected in the glio-interstitial tissue of the anterior byssus retractor muscle (ABRM) of Mytilus by the use of either dopamine or 5-HT as substrate and nitro blue tetrazolium salt as an electron receptor. Both substrates gave superimposable patterns. However, dopamine reactivity was very weak. Discrete but clear MAO activity was detected in the periphery of the smooth muscle cell, i.e., at the level of the peripherally localized mitochondria. The presence of MAO in the epithelium of the buccal palps was also demonstrated. These histochemical observations can be correlated with certain ultrastructural aspects, in particular the presence electron dense organelles profiles in glio-interstitial cells. This MAO activity is discussed in relationship with the high 5-HT content of ABRM and the control of its relaxation. Pigment formation and/or collagen tanning are discussed in terms of a possible relationship with inactivation of biogenic amines. These results complement previous data concerning the glio-interstitial tissue found in close association with muscle and nerve structures.

Animals↗

PubMedDate not supplied

[Separate and combined action of antibiotics and vitamins on monoamine oxidase activity of the rabbit liver in staphylococcal infection].

Staphylococcal necrotic infection decreases activity of mitochondrial monoamine oxidase from rabbit liver. The animals treated with tetracycline exhibited a further inhibition of staphylotoxin-repressed MAO activity. Administration of penicillin as well as of vitamins B2 and B12 resulted in the same level of the enzyme activity as in non-treated animals. Treatment of animals with tetracycline in combination with vitamins B2 and B12 ensured a restoration of MAO activity, repressed by antibiotics, to the level of non-treated animals. Combined administration of penicillin and methycillin with vitamins B2, as well as methycycline and morphocycline with vitamin B12 resulted in a higher enzyme activity compared with respective values in non-treated animals. The best stimulatory action was exerted by a combination of penicillin with vitamin B2 and methycillin with vitamin B12. In these cases, MAO activity was higher in rabbits receiving antibiotics only and was restored to the level of enzyme activity in intact animals. Combined administration of penicillin with vitamin B12 and morphocycline with vitamin B2 exerted no action on MAO activity inhibited by staphylococcal exotoxin.

Animals↗

PubMed2002

Platelet monoamine oxidase activity in a nonhuman primate model of type 2 excessive alcohol consumption.

OBJECTIVE: Low platelet monoamine oxidase (MAO) activity is associated with "type 2 alcoholism." MAO activity is also affected by cigarette smoking. Since most alcoholics are smokers, it is difficult to evaluate the possible effect of platelet MAO activity on alcoholism independently of the effects of smoking. The authors investigated the relationship between platelet MAO activity and excessive alcohol consumption in rhesus macaques. METHOD: Platelet MAO activity and CSF metabolite concentrations were measured. The authors also investigated level of voluntary alcohol intake and social dominance rank. RESULTS: Subjects with low platelet MAO activity consumed alcohol to excess, had low CSF 5-hydroxyindoleacetic acid concentrations, and were less competent socially. CONCLUSIONS: These findings show that nonhuman primates that exhibit type 2-like alcohol features display low platelet MAO activity and support the notion that platelet MAO activity is a biologic marker for central serotonergic activity. The results also challenge the hypothesis that low platelet MAO activity in type 2 alcoholism is simply an artifact of smoking.

Alcohol Drinking↗

PubMed2002

Increase in expression of brain serotonin transporter and monoamine oxidase a genes induced by repeated experience of social defeats in male mice.

Serotonin transporter and monoamine oxidase (MAO) A are involved in the inactivation of serotonin. The former is responsible for serotonin re-uptake from the synapse, whereas the latter catalyzes serotonin deamination in presynaptic terminals. Expression of serotonin transporter and MAO A genes was investigated in raphe nuclei of midbrain of CBA/Lac male mice with repeated experience of social victories or defeats in 10 daily aggressive confrontations. The amount of cDNA of these genes was evaluated using multiplex RT-PCR. Two independent experiments revealed that the defeated mice were characterized by significantly higher levels of serotonin transporter and MAO A mRNAs than the control and aggressive animals. Increased expression of MAO A and serotonin transporter genes is suggested to reflect the accelerated serotonin degradation in response to activation of the serotonergic system functioning induced by social stress. Significant positive correlation between MAO A and serotonin transporter mRNA levels suggests common pathways of regulation of transcriptional activity of these genes.

Aggression↗

PubMed1982

Effects of local anesthetics on monoamine oxidase, and their membrane effects.

The effects of various local anesthetics on rat brain and liver monoamine oxidase (MAO) and their antihemolytic and local anesthetic effects were studied. All local anesthetics tested at 1 x 10(-7) M to 1 x 10(-3) M inhibited MAO activity in rat liver mitochondria with 5-hydroxytryptamine (5-HT) as substrate. The order of potency was tetracaine>procaine>dibucaine>lidocaine>prilocaine. Tetracaine and procaine inhibited 5-HT oxidation much more than beta-phenylethylamine (PEA) oxidation. Dibucaine inhibited PEA oxidation as much as 5-HT oxidation. Inhibition of MAO by local anesthetics other than dibucaine was reversible. Tetracaine and procaine inhibited 5-HT oxidation competitively, whereas dibucaine inhibited it non-competitively. Antihemolytic effects were observed with dibucaine and tetracaine at concentrations of 6 x 10(-5) M and 1 x 10(-4), respectively. The order of surface anesthetic potencies was dibucaine>tetracaine>prilocaine>lidocaine>procaine. These results suggest that the inhibition of MAO activities by local anesthetics depends on both electrostatic and hydrophobic interactions between these drugs and enzyme-associated phospholipids or the hydrophobic regions of proteins.

Anesthetics, Local↗

PubMed2001

Substrates but not inhibitors alter the redox potentials of monoamine oxidases.

The midpoint potentials for the reduction of the cysteinyl-flavin adenine dinucleotide (FAD) in monoamine oxidases (MAO) A and B in the absence and presence of ligands have been determined. Both MAO A and MAO B can be reduced chemically in two steps, the first generating a semiquinone spectrum and the second the spectrum of fully reduced FAD, each of which requires two electron equivalents. The midpoint potentials for the oxidized/semiquinone and semiquinone/reduced couples were -159+/-4 mV and -262+/-3 mV for MAO A and -167+/-4 mV and -275+/-3 mV for MAO B. After modification with a thiol reagent, direct reduction from the oxidized to fully reduced form was observed with no semiquinone and without change in the overall midpoint potential. In the presence of substrate, no semiquinone was formed, but the midpoint potential for full reduction of the flavin was positively shifted by up to 500 mV, depending on the substrate. This shift in potential could permit a more thermodynamically favorable transfer of electrons from the amine substrates to oxygen. In contrast, stable products and inhibitors did not cause a shift in potential and did not prevent the formation of semiquinone.

Disulfides↗

PubMedDate not supplied

Monoamine oxidase isoenzymes in rat brain: differential changes during postnatal development but not aging.

Differential development of monoamine oxidase (MAO) isoenzymes in rat whole brain is described in postnatally developing Sprague-Dawley rats. Total MAO and isoenzyme activity was measured using nonspecific and specific substrates. Total MAO activity measured using tyramine, increased postnatally up to 24 weeks of age and attained a plateau afterward. The increase in total MAO activity was significant at all age groups (18 days to 36 months) investigated as compared to new born rats. MAO-A and MAO-B activities were measured using octopamine and benzylamine respectively. We also observed a marginal increase of MAO-A activity and a significant increase of MAO-B activity upon development. Furthermore, at 12 weeks of age, MAO-B activity increased by 10-fold as compared to new born and was consistent up to 36 months of age. The qualitative localization of the enzyme activity on non SDS-PAGE by nitroblue tetrazolium staining confirmed the increase of MAO-B during the development. It is suggested that the maturational increase of total MAO activity in brain is predominantly due to the increase of MAO-B isoenzyme.

Aging↗

PubMed1995

Effects of deprenyl on monoamine oxidase and neurotransmitters in the brains of MPTP-treated aging mice.

Deprenyl is a selective monoamine oxidase B (MAO-B) inhibitor and has been used in the treatment of Parkinson's disease. However, it is not known whether deprenyl effects are symptomatic or pharmacological. Aging mice were partially lesioned with MPTP. Control and MPTP-treated mice were given deprenyl in drinking water for 14 days. Brain tissue (including the striatum, olfactory tubercle and cerebral cortex) was assayed for MAO-B and neurotransmitter levels. The results show that deprenyl treatment, given alone or after MPTP, reduced MAO-B activity in all the three regions. No change was seen in dopamine (DA), 3,4-dihydroxyphenyl acetic acid (DOPAC), and homovanillic acid (HVA) content in any of the three areas. Cortical norepinephrine (NE) levels were also unaltered. However, striatal serotonin (5-HT) levels were decreased while its metabolite, 5-HIAA levels were significantly increased in the olfactory tubercle in animals receiving deprenyl alone. These data suggest that deprenyl treatment reduces MAO-B activity in regions in addition to the striatum without affecting norepinephrine, dopamine (DA) and its metabolites.

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

PubMed1986

Monoamine receptor sensitivity changes following chronic administration of MDL 72394, a site-directed inhibitor of monoamine oxidase.

(E)-beta-Fluoromethylene-m-tyrosine (MDL 72394) is not per se an inhibitor of monoamine oxidase (MAO) but is a substrate of aromatic L-amino acid decarboxylase (AADC) which liberates the potent MAO inhibitor (E)-beta-fluoromethylene-m-tyramine (MDL 72392). When co-administered to animals with the peripherally selective AADC inhibitor, carbidopa, MDL 72394 inhibited MAO selectively in the brain. Chronic (14 days plus 3 days withdrawal) administration of 0.5 mg/kg per day p.o. MDL 72394, 0.1 mg/kg per day p.o. MDL 72394 combined with 10 mg/kg per day p.o. carbidopa or 50 mg/kg per day p.o. pargyline produced equivalent inhibition of rat brain MAO and decreased the binding of [3H]clonidine and [3H]RX 781094 to the alpha 2-adrenoceptor and of [3H]dihydroalprenolol to the beta-adrenoceptor without changing binding of [3H]prazosin to the alpha 1-adrenoceptor. The locomotor depressant effect of clonidine was attenuated without attenuation of the hypotensive effect in rats treated chronically with the MAO inhibitors. Neither the sensitivity of the alpha 2-autoreceptor nor of the alpha 2-heteroreceptor was decreased in brain slices. However, the sensitivity of adenylate cyclase to activation by both noradrenaline and isoprenaline was significantly reduced. The number of 5-HT2 and 5-HT1A binding sites was decreased: the 5-HT1B binding sites remained unchanged. The effect of chronic MAO inhibitor treatment on 5-HT1A receptors was associated with a decrease in the behavioural response to 8-hydroxy-2-(di-n-propylamino)tetralin and the decrease in 5-HT2 binding was related to a small reduction in the sensitivity of the inositol phosphate system to stimulation by 5-HT. The lack of effect of chronic MAO treatment on the 5-HT autoreceptor measured in cortical slices corresponded to a lack of effect on the 5-HT1B binding site except that chronic administration of pargyline produced a small but significant decrease in 5-HT autoreceptor sensitivity. Overall, the data show that chronic administration of MDL 72394 has a profile of effects on central monoamine receptor binding and function similar to that seen following chronic administration of a number of clinically effective antidepressants.

Adenylyl Cyclases↗

PubMed1991

Use of pig hepatocytes to study the inhibition of monoamine oxidase by furazolidone.

Primary cultures of pig hepatocytes were used to examine the irreversible inhibition of monoamine oxidase (MAO), which has been observed in tissues of a number of different animal species after oral treatment with furazolidone. The rapid biotransformation of the MAO substrate p-tyramine by intact cells could effectively and irreversibly be inhibited with the known MAO inhibitors iproniazid and clorgyline. Incubation of cells with beta-hydroxyethylhydrazine and also 3-amino-2-oxazolidinone, which were previously proposed as the metabolites of furazolidone responsible for the in vivo effect, resulted in an irreversible inhibition of the MAO activity. Incubation of cells with furazolidone also resulted in a dose-related inhibition, but this effect was completely reversible on withdrawal of the drug. A similar MAO inhibition was observed after treatment of cells with nitrofurazone and furaltadone but not with nitrofurantoin. The results obtained with intact cells were confirmed by studies with 13,000 g pellets of homogenates made from cells preincubated for 24 hr with the compounds, which showed an irreversible inhibition in the case of iproniazid and 3-amino-2-oxazolidinone, but not in the case of furazolidone. The present study shows that hepatocytes are capable of transforming 3-amino-2-oxazolidinone, but not furazolidone itself, into a potent irreversible type of MAO inhibitor.

Animals↗

PubMed1998

Effect of T-2 toxin on blood-brain barrier permeability monoamine oxidase activity and protein synthesis in rats.

Systemic exposure to T-2 toxin disrupts brain biogenic monoamine metabolism. Although the mechanisms underlying these neurochemical perturbations are unclear, we have suggested that they are a reflection of increased blood-brain barrier (BBB) permeability, or altered protein synthesis that affects brain enzyme activities. Accordingly, BBB permeability, in vitro protein synthesis and in vitro monoamine oxidase (MAO) activity were examined in rats after either acute, or 7-day exposure to T-2. Membrane permeability was assessed from the recovery of systemically administered [14C]mannitol and [14C]dextran with [3H]water as the diffusible reference, either 2 hr post-intraperitoneal (i.p.) injections of 0, 0.2 and 1 mg T-2/kg body weight or following a 7-day exposure to diets containing 0 and 10 ppm T-2. Protein synthesis, determined by [14C]leucine incorporation, and MAO activity, determined by H2O2 production, were observed either 2 hr post-ip injection of 0 and 1 mg T-2/kg body weight or following a 7-day exposure to diets containing 0, 2.5 and 10 ppm T-2. Permeability increases were observed in all brain regions examined for mannitol, but not for dextran following T-2 i.p. The effect of dietary T-2 was more modest, affecting mannitol uptake in two brain regions, the cerebellum and pons plus medulla regions. Protein synthesis was significantly decreased by i.p. administration of T-2, while dietary treatment significantly reduced MAO enzyme activity. Collectively, the effect of T-2 toxin on BBB permeability, protein synthesis and MAO enzyme activity may account for the neurochemical imbalance observed in T-2 intoxication.

Animals↗

PubMed1985

Vascular monoamine oxidase activity in the rat brain: variation with the substrate and the vascular segment.

Brain vascular monoamine oxidase (MAO) was assayed in order to determine (a) whether microvessel MAO is more or less specific for certain substrates and (b) if the extraparenchymal, pial arteries possess an MAO activity as high as that in the microvessels. Rat brain microvessels were prepared by gentle homogenisation of grey matter, followed by filtration and differential centrifugation of the matter retained. Pial arteries were carefully freed of the meninges and cut into small segments. For comparison, rat mesenteric arteries were also dissected out and cut up. MAO was assayed by measuring the rate of oxygen consumption in a small cell with a Clark electrode. Although a high microvessel MAO activity (2.2 +/- 0.3 nmol min-1 mg prot.-1) was found using noradrenaline as substrate, significantly higher rates were found with tyramine, serotonin and beta-phenyl-ethylamine. By contrast, both pial and mesenteric arteries showed a 6-7 fold lower activity (substrate tyramine). These results indicate first, that a certain specialisation of the microvessel MAO activity exists which is apparently independent of the classical A or B-form category of the substrates, and second, that the extraparenchymal vessels (pial arteries) appear to possess significantly lower MAO activity, in accordance with the concept that blood-brain properties are induced by the cerebral parenchyma.

Animals↗

PubMed1985

Biochemistry and physiology of monoamine oxidase (MAO) activity in the ring dove (Streptopelia risoria). II. Distribution of MAO in different tissues.

Monoamine oxidase (MAO) activity was measured fluorometrically in liver, kidney, intestine and brain of adult male and female ring doves. Liver MAO was inhibited in a concentration-related fashion by clorgyline and harmaline (MAO type A inhibitors) where a plateau in the inhibition curve occurred with about 15% activity remaining, and also by the type B inhibitor deprenyl, which produced a plateau when about 85% activity remained. Kidney, intestine and brain MAO were inhibited in a biphasic manner by harmaline. Results with inhibitors suggest that 85% of liver MAO, 86% of kidney MAO, 88% of intestine and 75% of brain MAO is type A. Using 10(-6) M harmaline to differentiate between MAO-A and MAO-B type activities, the apparent maximal velocities (Vmax) and Michaelis constants (Km) were determined in different tissues. Most activity occurred in the intestine, with proportionally lesser amounts of kidney, liver and brain. The majority of MAO present was in the A form. Except for kidney, Km of MAO-B was higher than that of MAO-A. Both MAO-A and -B activities were higher in the intestines of male birds, although sex differences in content and type of MAO activity were not observed in other tissues of the ring dove.

Animals↗

PubMed1987

Mapping human brain monoamine oxidase A and B with 11C-labeled suicide inactivators and PET.

The regional distributions of monoamine oxidase (MAO) types A and B have been identified in human brain in vivo with intravenously injected 11C-labeled suicide enzyme inactivators, clorgyline and L-deprenyl, and positron emission tomography. The rapid brain uptake and retention of radioactivity for both 11C tracers indicated irreversible trapping. The anatomical distribution of 11C paralleled the distribution of MAO A and MAO B in human brain in autopsy material. The corpus striatum, thalamus, and brainstem contained high MAO activity. The magnitudes of uptake of both [11C]clorgyline and L-[11C]deprenyl were markedly reduced in one subject treated with the antidepressant MAO inhibitor phenelzine. A comparison of the brain uptake and retention of the 11C-labeled inactive (D-) and active (L-) enantiomers of deprenyl showed rapid clearance of the inactive enantiomer and retention of the active enantiomer within MAO B-rich brain structures, in agreement with the known stereoselectivity of MAO B for L-deprenyl. Prior treatment with unlabeled L-deprenyl prevented retention of L-[11C]deprenyl. Thus, suicide enzyme inactivators labeled with positron emitters can be used to quantitate the distribution and kinetic characteristics of MAO in human brain structures.

Adult↗

PubMed1981

Gonadal influences on the sexual differentiation of monoamine oxidase type A and B activities in the rat brain.

The sex-dependent differentiation of monoamine oxidase (MAO) in the hypothalamus of 60-day-old, Charles River rats was found to involve only type A (MAO-A), and not type B (MAO-B) enzyme. In vivo inhibition of type A by clorgyline, and type B by (--)deprenyl, however, tended to decrease the specific activity of both types of MAO to a smaller extent in the female than in the male hypothalamus. When masculinization was prevented by neonatal administration of estradiol (E) to males, hypothalamic MAO-A and MAO-B activities increased in both control and MAO-inhibited rats. Androgenization of females, however, had little effect on the MAO activity. Whereas the effects of neonatal estrogenization were attributable neither to a direct influence of E nor to a sexual difference in the peripheral clearance of the MAO-inhibitor used, single, high doses of steroids to adult, but not to newborn rats, did acutely affect the kinetics of MAO-A. The activity of MAO-A was also decreased by high concentrations of E or TS in vitro. The imprinting for patterns of hypothalamic MAO-A and MAO-B in the two sexes results, probably, from genetic predetermination. Neonatal changes in the homeostasis of gonadal hormones may result in type-MAO nonspecific effects in adulthood, whereas the short-term effects of high concentrations of steroids may be selective for the A form.

Animals↗