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PubMed1994

Criminality and platelet monoamine oxidase activity in former juvenile delinquents as adults.

Platelet monoamine oxidase (MAO) activity was estimated in 70 former delinquent boys and 40 controls now aged 38-46 years. Platelet MAO activity was compared with their early criminal behaviour (before the age of 15) and their late registered criminality from the age of 15). Mean platelet MAO activity in subjects with both early and late criminality was significantly lower than that in former delinquents without late criminality. There was no significant difference in mean platelet MAO activity between controls and delinquents with early but no late criminality. When delinquents with early criminality were divided into a low and a high MAO group, the relative risk to be registered for late criminality was about 3.1 times higher for the subjects in the low MAO group. Thus, individuals with low platelet MAO activity run an increased risk of continued criminal behaviour.

Adolescent↗
PubMedDate not supplied

[Defect in the properties of brain mitochondrial monoamine oxidase in schizophrenia].

A highly purified individual form of monoamine oxidase (MAO-11b) has been isolated by means of affinity chromatography on AH-Sepharose 4B after solubilization of biomembranes from schizophrenic or normal brain tissues. The enzyme preparations obtained catalyzed deamination (both in schizophrenia and normal state) not only of serotonin and 2-phenylethylamine but also of histamine and contained about 2 SH-groups per 10(5) dalton of protein which is characteristic for "transformed" MAO with partially oxidized SH-groups. Preincubation of MAO-11b from normal brain with 10 mM dithiothreitol caused "re-transformation" of MAO: there was a marked decrease in histamine deaminating activity with simultaneous increase in the MAO activity and in content of SH-groups. In schizophrenia the re-transformation of MAO was impaired: preincubation of MAO-11b under the same conditions led to an increase in content of SH-groups and in MAO activity but the preincubation with a reducing agent did not decrease (causing, to the contrary, a marked increase) the deamination of histamine.

Brain↗
PubMed2004

Both low and high activities of platelet monoamine oxidase increase the probability of becoming a smoker.

Platelet monoamine oxidase (MAO) activity is a marker of personality and psychiatric vulnerability, but the direct inhibitory action of tobacco constituents on the enzyme distorts the association. In the present investigation, data from a prospective longitudinal study of smoking behaviour and platelet MAO activity in adolescents at ages 15 and 18 years were sequentially analysed using a second-order multiple logistic regression analysis. The odds of regular smoking at 18 years increased significantly with increasing absolute deviation of platelet MAO activity at 15 years from the mean. That is, both low and high platelet MAO activity at 15 years predicted a higher probability of becoming a smoker. These data suggest that smoking is associated with low platelet MAO activity not only because of the direct inhibitory effect of tobacco constituents on the enzyme, but also because subjects with low platelet MAO activity are more likely to become smokers. Furthermore, the possible association between above-average platelet MAO activity and behavioural phenotypes should be reexamined.

Adolescent↗
PubMed1992

Peripheral blood cell activities of monoamine oxidase B and superoxide dismutase in Parkinson's disease.

Monoamine oxidase type B (MAO-B) and superoxide dismutase (SOD) are two enzyme systems that are potentially relevant to an oxidative stress model of Parkinson's disease (PD) causation. Activities of MAO-B in platelets (nmol/10(8) cells/hr) and total SOD in lymphocytes (U/mg protein) were assayed among 28 cases of idiopathic PD and 22 controls. As anticipated, MAO-B was lowest in PD cases on selegiline (L-deprenyl) therapy (mean 1.10). There was a slight deficit of MAO-B among male cases not taking selegiline compared to controls (3.78 vs. 4.15), but the opposite trend was observed for females (6.18 vs. 4.16). SOD was slightly higher in cases (7.40), than controls (6.81). Excess SOD among PD cases was seen irrespective of gender, age, or selegiline treatment, although none of the differences was statistically significant. Future research on SOD should take advantage of the availability of assays specific for the cytosolic and mitochondrial forms of the enzyme.

Adult↗
PubMedDate not supplied

Some cardiovascular effects of monoamine oxidase inhibitors in unanaesthetized rats.

The effects of four monoamine oxidase (MAO) inhibitors on the blood pressure of conscious normotensive and DOC-salt hypertensive rats were measured. Harmaline (20 mg/kg p.o.), pargyline (100 mg/kg p.o.) and tranylcypromine (10 mg/kg p.o.) all lowered blood pressure significantly in both normotensive and hypertensive rats whereas methylaplysinopsin (10 mg/kg p.o.) had no effect on blood pressure. The effects of these MAO inhibitors on blood pressure responses to serotonin, tyramine and beta-phenylethylamine were determined in conscious normotensive rats. Pargyline and tranylcypromine shifted the dose-response curves for tyramine and beta-phenylethylamine, but not serotonin, to the left, indicating inhibition of type B MAO. Harmaline and methylaplysinopsin shifted the dose-response curves for tyramine and serotonin but not beta-phenylethylamine, to the left, indicating inhibition of type A MAO. Since the four antagonists tested inhibited at least one form of MAO, and yet not all of these MAO inhibitors lowered blood pressure, we suggest that our results are consistent with the view that the hypotensive action of MAO inhibitors is not necessarily related to inhibition of MAO.

Anesthesia↗
PubMed1991

Simultaneous delivery of valproic acid and glycine to the brain. Deamination of 2-propylpentylglycinamide by monoamine oxidase B.

2-Propylpentylglycinamide (2-PPG), a branched aliphatic amine derivative, was found to be readily deaminated by rat liver monoamine oxidase B in vitro and in vivo. The deamination leads to production of 2-propyl-1-pentaldehyde, which can be subsequently converted to valproic acid (VPA), and glycinamide, which is then subsequently converted to glycine. Absorption and biotransformation of a single ip dose of 2-PPG into blood as well as transfer of the drug and its metabolite into the brain were rapid processes. Although VPA (an anticonvulsant) and glycine (an inhibitory neurotransmitter) can be detected in the brain following administration of 2-PPG, its anticonvulsant action cannot be determined. 2-PPG at relatively low doses exhibited distinct tremor effects. Furthermore, 2-PPG appeared to potentiate the convulsant effect induced by pentylenetetrazol.

Animals↗
PubMed2004

Haplotypes of the monoamine oxidase genes and the risk for substance use disorders.

Monoamine oxidase A (MAOA) locus is an attractive candidate for exploring genetic contribution to the variation in the risk for substance use disorders (SUD) because of its important role in the metabolism of neurotransmitters, including dopamine and serotonin. Prior findings have suggested an association of the MAOA gene with the risk for early onset SUD. To extend this research, we genotyped four MAOA markers (two VNTR polymorphisms and two SNPs) and built a cladogram reflecting the evolutionary history of MAOA haplotypes [Nguyen et al., under review]. The cladogram served as the framework for nested ANOVA and logit analyses of association between MAOA and indices of liability to SUD (diagnosis, age of onset, and a dimensional index of substance use related problems) in a sample of adult males of European ancestry. Whereas no association was found for the categorical diagnosis, a significant relationship was detected between the dimensional liability indices and MAOA haplotypes. Overall, our results, albeit not definitive, are consistent with the hypothesis that variants in MAOA account for a small portion of the variance of SUD risk, possibly mediated by liability to early onset behavioral problems.

Adult↗
PubMed1985

Pentametric distribution of platelet monoamine oxidase activity.

The distribution of catalytic activity of platelet monoamine oxidase (MAO) with both tryptamine and phenylethylamine as substrates was examined in 1,129 Swedish men at age 18 years. A mixture of five components was needed to describe the distribution, even when the original scale was transformed to remove skewness. The proportions of admixture were 2% for the extremely low component with a mean of -2.3 sigma, 29% for moderately low MAO (mean -0.8 sigma), 51% for intermediate MAO (mean 0.0 sigma), 15% for moderately high MAO (mean + 1.3 sigma), and 3% for extremely high MAO (mean + 3.0 sigma). Thus, the upper and lower deciles each contain contributions from two extreme components that differ from a much larger intermediate component with activity near the mean of the general population. This is compatible with a minimum of three alleles at a single major locus or with at least two polymorphic loci. The hypothesis that MAO activity is controlled by two alleles at a single locus was tested and rejected. The demonstration of at least five distinct components to the distribution of MAO warrants further research to characterize the biochemical structure and function of MAO enzyme variants as well as study of the behavioral correlates of the components.

Adolescent↗
PubMed2000

Platelet monoamine oxidase activity is related to MAOB intron 13 genotype.

Monoamine oxidases (MAO) play a critical role in the degradation of endogenous and exogenous amines throughout the body. There are two distinct MAO isoforms, MAO-A and MAO-B, which both are encoded in genes on the X chromosome. Alterations in MAO-B activity have previously been connected with several neurological disorders. Platelet MAO (trbc-MAO) is exclusively of the B-type and the catalytic activity of this enzyme is under strong, yet unknown, genetic control. Specific trbc-MAO activity has been reported to be increased in certain neurodegenerative diseases and to correlate with personality traits such as sensation seeking and impulsiveness. In the present study, we investigated if trbc-MAO activity is associated with genotype at a variable region (A/G dimorphism) in intron 13 of the human gene encoding MAO-B. The MAOB intron 13 allele status and levels of trbc-MAO were determined for 55 Caucasian non-smoking males. Individuals with the "A-allele" displayed significantly lower enzyme activity than individuals with the "G-allele", i.e. 11.4 +/- 0.6 nmol/10(10) platelets/min compared with 13.5 +/- 0.6 (mean +/- SEM, p = 0.019). The present results suggest that the MAOB genotype may be involved in determining trbc-MAO activity.

Adult↗
PubMed1981

Tyramine antagonistic properties of AGN 1135, an irreversible inhibitor of monoamine oxidase type B.

1 The effects of the irreversible monoamine oxidase (MAO) inhibitors, AGN 1133, AGN 1135 and (-)-deprenyl, on tyramine and noradrenaline responses and uptake of [3H]-metaraminol were investigated in the isolated vas deferens of the rat. Uptake of [3H]-metaraminol and [3H]-octopamine was compared in mouse vas deferens. The modification of tyramine and noradrenaline-induced pressor responses by AGN 1133 and AGN 1135 was examined in anaesthetized rats and cats. 2 AGN 1133 (7.5 x 10(-6)M) greatly potentiated responses to tyramine in the rat isolated vas deferens. Both AGN 1135 and (-)-deprenyl inhibited tyramine responses selectively at concentrations above 10(-5)M (which caused almost complete inhibition of MAO types A and B) but tyramine responses were potentiated on washing out the inhibitors. 3 AGN 1135 (10(-4)M) and (-)-deprenyl (10-5)M) inhibited [3H]-metaraminol uptake by about 20% in rat and mouse vas deferens; neither inhibitor affected [3H]-octopamine uptake in mouse vas deferens. Desmethylimipramine (10(-6)M) inhibited amine uptake by more than 70%. 4 AGN 1133 (1.5 mg/kg) potentiated pressor responses to tyramine in rats and cats whereas AGN 1135 (1.5 mg/kg) did not. 5 AGN 1135 possesses tyramine antagonistic activity which is qualitatively similar to that of (-)-deprenyl but which cannot satisfactorily be explained by inhibition of neuronal or granula amine uptake.

Animals↗
PubMed1985

Platelet-monoamine oxidase activity in Reye's syndrome.

Platelet and liver monoamine oxidase (MAO) activity (mean +/- SD) was evaluated in patients with liver-biopsy-proven Reye's syndrome. MAO was measured by a radioenzymatic technique with [3H]tyramine as a substrate. A marked decrease in MAO activity [3.3 +/- 2.4 nmol of [3H]4-hydroxyphenylacetic acid formed X (mg protein)-1 X h-1] was observed in platelets on admission in all patients (n = 13) with Reye's syndrome when compared with hospitalized patients without liver disease (n = 8) [9.8 +/- 2.5 nmol of [3H]4-hydroxyphenylacetic acid formed X (mg protein)-1 X h-1] and with liver disease (n = 10) [9.1 +/- 2.0 nmol of [3H]4-hydroxyphenylacetic acid formed X (mg protein)-1 X h-1]. Following recovery from the disease, platelet MAO approached levels that were not significantly different from those of controls. Contrastingly, reduction of hepatic MAO in Reye's syndrome was similar to that seen in patients with liver disease of different etiologies. These studies suggest that reduced platelet MAO activity is a specific abnormality in Reye's syndrome, and it may be representative of generalized impairment of mitochondrial function in these patients. Furthermore, the pattern of liver and platelet MAO activity in Reye's syndrome may allow for the differentiation of this disease from other hepatopathologic conditions.

Adolescent↗
PubMed1993

Hydrogen peroxide production by monoamine oxidase during ischemia-reperfusion in the rat brain.

Monoamine oxidase (MAO) as a source of hydrogen peroxide (H2O2) was evaluated during ischemia-reperfusion in vivo in the rat brain. H2O2 production was assessed with and without inhibition of MAO during and after 15 min of ischemia. Metabolism of H2O2 by catalase during ischemia and reperfusion was measured in forebrain homogenates using aminotriazole (ATZ), an irreversible H2O2-dependent inhibitor of catalase. Catecholamine and glutathione concentrations in forebrain were measured with and without MAO inhibitors. During ischemia, forebrain blood flow was reduced to 8% of baseline and H2O2 production decreased as measured at the microperoxisome. During reperfusion, a rapid increase in H2O2 generation occurred within 5 min as measured by a threefold increase in oxidized glutathione (GSSG). The H2O2-dependent rates of ATZ inactivation of catalase between control and ischemia-reperfusion were similar, indicating that H2O2 was more available to glutathione peroxidase than to catalase in this model. MAO inhibitors eliminated the biochemical indications of increased H2O2 production and increased the catecholamine concentrations. Mortality was 67% at 48 h after ischemia-reperfusion, and there was no improvement in survival after inhibition of MAO. We conclude that MAO is an important source of H2O2 generation early in brain reperfusion, but inhibition of the enzyme does not improve survival in this model despite ablating H2O2 production.

Amitrole↗
PubMed2001

Regulation of human monoamine oxidase B gene by Sp1 and Sp3.

The human monoamine oxidase (MAO) B plays a major role in the degradation of biogenic and dietary amines such as phenylethylamine, benzylamine, dopamine, and tyramine. We previously showed that the -246/-99 MAO B promoter region exhibited the highest activity and contained two clusters of overlapping Sp1 sites, a CACCC element and a TATA box. Here, using a series of 10 deletion constructs of the 2-kilobase pair 5'-flanking sequence, we identified additional potential regulatory elements, including activator proteins 1 and 4, CAAT, GATA, upstream stimulatory factor (USF), estrogen receptor (ER), and sex-determining region Y-box 5 (SOX5). Analysis of nine site-directed mutations of -246/-99 region reveals that both clusters of Sp1 sites contribute positively whereas the CACCC element contributes negatively to the transcriptional activity. Gel shift analysis demonstrates that in addition to Sp1, Sp3 can interact with both clusters of Sp1 sites. Cotransfection experiments show that Sp1 and its closely related family member Sp4 can trans-activate MAO B promoter activity through the proximal cluster of Sp1 sites and its activation can be repressed by the over-expression of Sp3 and a related family member BTEB2. These results suggest that the binding to the overlapping Sp1 sites by various members of Sp family is important for the regulation of the MAO B gene expression.

Base Sequence↗
PubMed2006

Childhood maltreatment, subsequent antisocial behavior, and the role of monoamine oxidase A genotype.

BACKGROUND: A functional promoter polymorphism in monoamine oxidase A (MAOA) has been implicated as a moderating factor in the relationship between childhood maltreatment and later adolescent and adult antisocial behavior. Despite wide interest in this hypothesis, results remain mixed from the few attempts at replication. METHODS: Regression-based analyses were conducted to test for a genotype-environment interaction using self-reported physical abuse and MAOA genotype to predict later antisocial behavior and arrests for violence by participants in the National Youth Survey Family Study. We also examined the interaction using a measure of violent victimization. The analysis sample included 277 Caucasian male respondents, aged 11-15 in 1976, who provided buccal swab DNA samples and who were successfully genotyped for the variable number tandem repeat (VNTR) in the MAOA promoter using polymerase chain reaction. RESULTS: Maltreatment by a parent during adolescence was a risk factor for adolescent and adult antisocial and violence related behavioral problems. Tests for the main effect of MAOA and a MAOA-maltreatment interaction were nonsignificant. Similar results were obtained using the measure of adolescent violent victimization. CONCLUSIONS: Findings from this general population sample could not confirm the hypothesis that MAOA moderates the relationship between adolescent maltreatment and adolescent or adult antisocial behavior.

Adolescent↗
PubMed1989

Characterization and quantitation of monoamine oxidases A and B in mitochondria from human placenta.

Monoamine oxidases (MAOs) A and B, flavin-containing enzymes found in the outer mitochondrial membrane, oxidize many important biogenic and xenobiotic amines. The two enzymes are expressed in many tissues, with some tissues containing primarily one form and others containing both. Although MAO in placental mitochondria is widely reported to be type A, some investigators have reported low levels of MAO B activity as well. Because placenta is considered the preferred source for purification of type A MAO, we have reinvestigated placental MAO by immunoblotting with monoclonal antibodies and active site labeling with the MAO-specific ligand [3H]pargyline. We have confirmed that placental mitochondrial preparations contain MAO A and low but significant MAO B catalytic activity, as judged by accepted pharmacological criteria (deprenyl-sensitive beta-phenylethylamine and benzylamine oxidation). Immunoblotting revealed polypeptides of sizes expected for both MAO A and B subunits in preparations of placental mitochondria, as well as in preparations of MAO A purified extensively from placenta by partitioning between dextran and polyethylene glycol polymers and chromatography on DEAE-Sepharose CL-6B. Both MAO A and B active sites could be quantitated in placenta by labeling mitochondrial preparations with the MAO-specific affinity ligand [3H] pargyline, followed by immunoprecipitation with MAO A- and MAO B-specific monoclonal antibodies. These results indicate that MAO B activity and protein is consistently present in mitochondrial preparations of human placenta.

Binding Sites↗
PubMed1987

Neuropsychological correlates of platelet monoamine oxidase (MAO) activity in female and male subjects.

Platelet monoamine oxidase (MAO) activity has been found to have behavioral (psychiatric and personality) correlates and is assumed to be linked to central transmitter systems and thus presumably to neuropsychological processes. In the present study, computerized neuropsychological tests, a reaction time (RT) test and a visuo-spatial problem solving test, the Perceptual Maze Test (PMT), were given to 32 female and 29 male students, each sex group divided into three subgroups on the basis of platelet MAO activity. The tests yield measures of laterality (reaction time for left- versus right-sided stimuli) and different aspects of cognitive strategy and skill, e.g. time used for inspection of the maze, for processing the stimulus pattern, and for checking the correctness of solutions. Low MAO female subjects had shorter RTs, pronounced for left-sided stimuli, and shorter inspection times in the PMT compared to other female subjects. Low and high MAO males had difficulties in inhibiting responses, when required, and low MAO males were more rapidly prepared to respond to new stimuli after short intervals than other males. In the PMT, high MAO male subjects spent a smaller part of the total time on inspection in relation to other male groups and had more rubouts than low MAO males, whose maze solving behavior indicated higher visuo-spatial ability. The results are discussed in terms of possible neurochemical bases of impulsivity and psychopathy, and of spatial skill.

Adolescent↗
PubMed1997

Genetic polymorphism of monoamine oxidase B and susceptibility of Parkinson's disease.

BACKGROUND: Monoamine oxidase B (MAO-B) may play a role in the progression and cause of Parkinson's disease (PD), given consideration of the biochemistry and pathophysiology of the disease, and experiments on primates and humans. Assuming that the structural gene determines enzyme activity, an association study was undertaken to examine MAO-B genetic polymorphisms and look for the unique MAO-B gene alleles which occurred at a higher frequency in PD patients. METHODS: Sixty-five PD patients, diagnosed according to the criteria set by a Core Assessment Program for Intracerebral Transplantations Committee, and 108 healthy controls were enrolled in this study. Genomic DNA was extracted from peripheral leukocytes by using a puregene kit. Polymerase chain reaction (PCR) was used to amplify the MAO-B genome. The PCR products were screened by restriction enzyme Hae III digestion and analyzed by single-stranded conformational polymorphism (SSCP). RESULTS: Two bands with different mobility shifts, defined as MAO-B allele 1 and allele 2, were observed in SSCP analysis. Neither genotypes nor allelic frequencies of MAO-B showed a significant difference between PD patients and controls in our study. CONCLUSIONS: Polymorphism of MAO-B genome was demonstrated in this study. It failed to show an association of a genetic marker with PD. However, this did not necessarily exclude the MAO-B locus from playing a role in causing PD because a polymorphism different from the one evaluated here may show some disease association.

Aged↗
PubMed1997

Inactivation of monoamine oxidase B by benzyl 1-(aminomethyl) cyclopropane-1-carboxylate.

Monoamine oxidase (MAO) is a flavoenzyme that catalyzes the oxidation of various biogenic and xenobiotic amines. Benzyl 1-(aminomethyl)cyclopropane-1-carboxylate (1) was designed as a diactivated cyclopropane mechanism-based inactivator of MAO (Silverman, R.B.: Ding, C.Z.; Borrillo, J.L.; Chang, J.T.J. Am. Chem. Soc. 1993, 115, 2982). [1,1-2H2]-1 exhibits a deuterium isotope effect of 4.5 on inactivation, but in D2O the isotope effect is only 2.3. [1-3H]-1 and [1-14C]-1 were synthesized; upon inactivation of MAO, 1.1 and 2.0 equiv of radioactivity, respectively, are incorporated into the enzyme. Tritium as 3H2O, is released during inactivation with [1-3H]-1. The flavin absorption spectrum changes from that of oxidized to that of reduced flavin after inactivation; denaturation of the inactivated enzyme shows a reduced flavin spectrum, suggesting the formation of a modified flavin. Tryptic digestion of the enzyme labeled with [1-3H]-1 or [1-14C]-1, followed by HPLC analysis, monitoring at 310 nm [corrected] (flavin), shows that the radioactivity comigrates with the 310 nm [corrected] absorptions. The metabolites that are generated during inactivation are benzyl 1-formylcyclopropane-1-carboxylate, benzyl alcohol, and 1-formylcyclopropane-1-carboxylic acid; no ring-cleaved products were detected. The partition ratio, as determined from the ratio of nonamines to enzyme, is 110. These results are rationalized in terms of a single-electron transfer mechanism leading to the imine of benzyl 1-formylcyclopropane-1-carboxylate, which alkylates the flavin coenzyme.

Amino Acids↗