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Effect of acute starvation on monoamine oxidase and Na+,K(+)-ATPase activity in rat brain.

The activities of monoamine oxidase (MAO), responsible for oxidative deamination of many biogenic amines, and Na+, K(+)-ATPase, which plays a crucial role in the release mechanism of neurotransmitters, were determined in rat brain after acute starvation. They were assayed biochemically from four different regions of the brain in two subcellular fractions. Acute starvation decreased the activity of MAO, whereas the Na+,K(+)-ATPase activity was increased. An effect of starvation was also seen on the blood glucose level, body wt, and the protein content of different brain regions. Starvation or normal dietary fluctuations of certain nutrients that exert precursor influence over neurotransmitter synthesis are important to the brain, and contribute to its regulation of both neuroendocrine response and behavior. A rise in the substrate level, i.e., ATP, as a result of increased utilization of ketone bodies and low level of monoamines in the brain after acute starvation, may be the underlying factor for increasing the activity of Na+,K(+)-ATPase in rat brain. These results suggest that, probably, certain adaptive mechanisms become operative in the brain under disturbed physiological conditions.

Acute Disease↗

A kinetic analysis of platelet monoamine oxidase activity in patients with panic attacks.

A kinetic analysis of platelet monoamine oxidase (MAO) was performed in 22 patients with panic disorder and 14 normal controls, using tyramine as a substrate. Patients and controls did not differ significantly for either Km or Vmax, when same sex contrasts were carried out. The results do not support some studies that have shown elevated MAO activity in patients with panic attacks. The reasons for the discrepancies between previous studies and the present one are explored.

Adult↗

Differential time course of protection by monoamine oxidase inhibition and uptake inhibition against MPTP neurotoxicity on central catecholamine neurons in mice.

Pretreatment with the monoamine oxidase inhibitor pargyline or the catecholamine uptake blocker nomifensine both protected central catecholamine neurons against MPTP-induced neurotoxicity as monitored by analyzing catecholamine levels and [3H]mazindol binding. Post-treatment with the inhibitors showed that the administration of nomifensine could be delayed longer than that of pargyline in order to achieve a protective effect. The results are compatible with the view that the monoamine oxidase-catalyzed conversion of MPTP to a toxic metabolite MPP+ occurs mainly extraneuronally. MPP+ is subsequently taken up and accumulated selectively in catecholamine neurons, initiating degeneration.

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

Platelet monoamine oxidase B activity and vitamin B12 in dementia.

The activity of platelet monoamine oxidase B (MAO-B) was highly correlated with the severity of dementia in 39 patients suffering from probable dementia of the Alzheimer type and in 18 age-matched controls. There was no association between a low vitamin B12 level and high MAO-B activity in our sample of patients, who are living in a geriatric hospital where the balanced nutrition of inpatients is controlled by diet assistants.

Aged↗

Selective inhibition of the "B form" of monoamine oxidase.

Deprenyl (phenyl-isopropyl-methyl-propinylamine) is a potent inhibitor of monoamine oxidase (MAO) and like the acetylenic type of inhibitors it induces irreversible inhibition of the enzyme. Its levorotatory isomer is a more potent inhibitor than the dextrorotatory one. Deprenyl elevates the concentration of 3H-noradrenaline (3H-NA) in the synaptosomal fraction of rat heart homogenate while pargyline, probably due to its releasing effect, decreases 3H-NA content in the same fraction. Deprenyl is a selective inhibitor of the "B form" of MAO, which preferentially oxidizes beta-phenylethylamine as substrate.

Animals↗

Platelet monoamine oxidase in families of chronic schizophrenics.

Many reports have described low platelet monoamine oxidase (MAO) activity in chronic schizophrenia. In an effort to determine whether this low activity is genetically controlled, the authors studied platelet MAO activity in the first-degree relatives of 12 chronic schizophrenics (who themselves had low platelet MAO activity). The 29 relatives had significantly lower mean Vmax and Km values than a control group. The authors postulate that the low platelet MAO activity among chronic schizophrenics may be a genetic marker for vulnerability to chronic schizophrenia.

Blood Platelets↗

Physiological and pathological changes in tissue monoamine oxidase activity.

This article explores the possibility that malfunction of the enzyme monoamine oxidase (E.C. 1.4.3.4., MAO) could lead to aberrations in the catabolism of biogenic amines in the central nervous system and give rise to certain mental abnormalities. No conclusive evidence could be presented to substantiate this. Data on the normal function of the enyzme (for example its existence in multiple forms, the control of MAO activity by hormones or the independent development of MAO activities towards different substrates during maturation) are reviewed.

Adrenal Glands↗

Cardiovascular changes in response to selective monoamine oxidase inhibition in the rat.

Chronic (21 days) treatment with the selective monoamine oxidase (MAO)-A inhibitor clorgyline, but not with the MAO-B inhibitor deprenyl in pithed rats leads to increased blood pressure responses to sympathetic stimulation and intravenous tyramine, and to elevated unstimulated heart rates. No significant changes are observed in plasma catecholamine responses to sympathetic stimulation, nor in beta-adrenoreceptor numbers in heart ventricles. These findings suggest that the hypotensive effects of MAO inhibitors result from central nervous system rather than peripheral nervous system alterations.

Animals↗

Some characteristics of monoamine oxidase activity in tissues of the adult female grassfrog (Rana pipiens).

1. Monoamine oxidase (MAO) activity was measured fluorometrically in tissues of the grass-frog, Rana pipiens. 2. Incubation with specific inhibitors revealed the presence of two forms of MAO, type A and type B, in all tissues examined, though the ratios were different in each tissue. 3. Liver contained the greatest, and oviduct and skeletal muscle the lowest amounts of MAO activity, and brain also contained relatively high MAO levels. 4. The apparent Michaelis constant (Km) was similar in most tissues but was higher in pancreas, muscle and oviduct. Values of Km were lower than those reported for mammalian tissues.

Animals↗

Monoamine oxidase B inhibitors from the fruits of Opuntia ficus-indica var. saboten.

Three varieties of methyl citrate and 1-methyl malate were isolated from the fruits of Opuntia ficus-indica var. saboten Makino through in vitro bioassay-guided isolation for the inhibition on monoamine oxidase(MAO). The IC50 values for MAO-B of 1-monomethyl citrate, 1,3-dimethyl citrate, trimethyl citrate and 1-methyl malate were 0.19, 0.23, 0.61 and 0.25 mM, respectively. However, on MAO-A, their inhibitions showed only marginal activity.

Citric Acid↗

Urinary output of endogenous monoamine oxidase inhibitor and isatin during acute migraine attacks.

Urinary output of endogenous monoamine oxidase (MAO) inhibitory activity, was significantly raised in serial samples collected across a migraine attack compared with collections during attack-free periods and in healthy controls, which did not differ from each other. There was a highly significant correlation in output between isatin, a major fraction of the MAO inhibitory activity, and output of the MAO inhibitory activity itself. However, although there was a tendency towards increased isatin excretion during migraine attacks, it failed to reach statistical significance.

Acute Disease↗

The characteristics and distribution of monoamine oxidase (MAO) activity in different tissues of the rainbow trout, Salmo gairdneri.

Monoamine oxidase (MAO) activity was determined fluorometrically in brain, intestine, kidney and liver tissues of the rainbow trout, Salmo gairdneri. MAO activity was inhibited by various drugs in a concentration-related manner, with single sigmoid inhibition curves, the inhibitors of type A MAO, harmaline and clorgyline being more effective than deprenyl, an inhibitor of type B MAO. Intestine exhibited greatest MAO activity followed by liver and brain with kidney showing least activity. The Michaelis constants (Km) also showed variability between tissues. Inhibition of MAO by harmaline was non-competitive and dependent on the concentration of substrate present.

Animals↗

Platelet monoamine oxidase activity and trace acid levels in plasma of agoraphobic patients.

Platelet monoamine oxidase activity and plasma trace acid levels in 29 patients classified as agoraphobics was estimated. MAO activity towards p-tyramine and beta-phenylethylamine was found to be significantly higher in agoraphobics than in non-agoraphobic depressed patients and healthy controls. In addition plasma p-hydroxyphenylacetic acid levels were low in both agoraphobic and depressed patient groups. All patients were also assessed by Spielberger State Anxiety and the short form of the Beck Depression Inventory scales. No significant correlations could be found between platelet MAO activity or plasma trace acid levels and the psychological scores.

Adult↗

Inhibition of monoamine oxidase by pirlindole analogues: 3D-QSAR and CoMFA analysis.

A series of pyrazinocarbazoles, analogues of short acting antidepressant pirlindole (2,3,3a,4,5,6-hexahydro-8-methyl-1H-pyrazino[3,2,1-j,k]carbazole hydrochloride), were tested as inhibitors of monoamine oxidase A (MAO-A) and B (MAO-B). Rigid analogues exhibited potent and selective inhibition of MAO-A and have size limits (X:Y:Z) of 13.0 x 7.0 x 4.4 A. Besides MAO-A inhibition flexible analogues also demonstrated potent inhibition of MAO-B and in contrast to rigid analogues their inhibitory activity did not show the dependence on these sizes. The qualitative information (steric and electrostatic coefficients) from the 3D-QSAR with CoMFA models for MAO-A and -B are different, and this information can be used to determine the structural features influencing inhibitor selectivity.

Animals↗

[Training and extinction of passive avoidance in mice lacking monoamine oxidase A].

The passive avoidance learning and memory trace retention in mice lacking monoamine oxidase A (MAO A) and control C3H strain were analyzed. It is shown that mice of both strains were well the passive avoidance learners. A delay of the memory trace extinction was found in lacking MAO A mice as compared with control C3H strain. Mice with a genetic MAO A knockout showed decreased amounts of transitions, rearings, looking to a dark compartment and appearing from it. These findings seem to reflect more expressed fear reaction to a dangerous compartment and increased anxiety promoting longer retention of memory trace on a high level of retrieval.

Animals↗

Investigation of a correlation between monoamine oxidase B and catechol-O-methyltransferase activity in human blood cells.

Monoamine oxidase B (MAO-B) and catechol-O-methyltransferase (COMT) are pivotal enzymes in the catabolism of several neurotransmitters. MAO-B and COMT activity can be reliably measured in human platelets and erythrocytes, respectively. This study investigated whether a correlation exists between the activity of the two enzymes in a panel of 47 elderly subjects (age range 55-80 years). No correlation was apparent between the two activities (r(2)<0.01), which suggests that, genetically, they are determined independently. COMT activity in a panel of 163 subjects showed a bimodal distribution with a nadir at approximately 38 pmol/h/mg Hb.

Adolescent↗

Monoamine oxidase in rat placenta, human placenta, and cultured choriocarcinoma.

The activity of monoamine oxidase (MAO), an enzyme which metabolized catecholamines and indoleamines, was determined in rat placenta at various stages of gestation, in human term placenta, and in choriocarcinoma grown in culture. From Day 15 to Day 20 of gestation the specific activity (units/mg protein) of MAO in rat placenta increased at least 3-fold; from Day 20 to the time of parturition, it decreased about 50%. The specific activity of MAO in human placenta at term was about 50%. The specific activity of MAO in human placenta at term was about 8 times higher than that of rat placenta at term. No MAO activity was found in choriocarcinoma grown in culture.

Animals↗

The effect of harmine and other monoamine oxidase inhibitors on N-acetyltransferase activity.

Prior studies indicate that the monoamine oxidase inhibitors (MAOI) harmine and iproniazide inhibit N-acetyltransferase activity from liver. In this report we have demonstrated that harmine and harmaline are potent inhibitors of N-acetyltransferase, purified from hamster and rat liver. However, other MAOI such as deprenyl, clorgyline, methysergide, cyproheptadine, phenelzine, pargyline, methyltryptamine and tranylcypromine have either no effect, or only trivial effects on N-acetyltransferase. There is no correlation between a compound's properties as an MAO and N-acetyltransferase inhibitor. One must consider the inhibitory effect of harmine and harmaline on both MAO and N-acetyltransferase when evaluating the effects of these compounds on physiological processes.

Acetyltransferases↗