Disease relevance of MAO

• Some of the clinical features of these MAO deletion patients may help to identify X-linked MAO deficiency diseases in humans [1].
• The mechanism of protection by MAO differs from that of CAO, because ganglion blockade abolished protection by MAO but not by CAO [2].
• We examined whether brief occlusion of the anterior mesenteric artery (MAO) or left renal artery (RAO) protects against myocardial infarction [2].
• Hypothermia (body temperature, 30 degrees C to 31 degrees C) did not affect IA/AR (67 +/- 3%, n = 11) in control animals but enhanced protection by 15-minute CAO (IA/AR = 22 +/- 3%, n = 8), whereas protection by 15-minute MAO (IA/AR = 44 +/- 5%, n = 11, P < .001) was minimally enhanced [2].
• A series of subclones prepared from a 'phage library (lambda DASH II) of the YAC have been characterised and have been employed to determine the end point of the deletion of a Norrie disease (NDP) patient who has been shown to lack both DXS7 and MAO coding sequences [3].

Psychiatry related information on MAO

• The decrease in skeletal muscle MAO activity in various types of psychotic patients is consistent with previous suggestions based on platelet studies that low MAO activity may be a nonspecific factor contributing to the development of different forms of psychopathology [4].
• The skeletal muscle MAO activity of schizophrenics and patients with bipolar and unipolar affective psychoses was lower than that of normal controls [4].
• Platelet MAO activity in primary degenerative dementia [5].
• Elevated platelet MAO activity in schizophrenia-related depressive disorders [6].
• The variables of sex, diagnosis, diurnal mood variation, platelet MAO activity, and MMPI scale scores were of minimal assistance in revealing factors that might be associated with activation or antidepressant responses to dextro-amphetamine in this small patient group [7].

High impact information on MAO

• The present study documents that a marked deficiency of MAO activity is compatible with life and that genes for MAO-A and MAO-B are near each other in this Xp chromosomal region [1].
• Platelet and plasma MAO activities were not correlated with skeletal muscle MAO activity [4].
• The present study provides evidence that the MAO genes are not disrupted in "classic" Norrie disease patients [8].
• The levels of dopamine are increased in the limbic brain areas of parkin mutant mice and there is a shift towards increased metabolism of dopamine by MAO [9].
• Localization of MAO-containing neurons, fibers and glial cells has been described by recent progress in MAO histochemistry and immunohistochemistry [10].

Chemical compound and disease context of MAO

• Succinylcholine and tricyclic and MAO-inhibiting antidepressants can precipitate malignant hyperthermia and were thus avoided [11].
• The third section, "Norepinephrine and Pharmacologic Treatment," briefly discusses the use of adrenergic blockers, clonidine and propranol, as well as tricyclic and MAO inhibitors, for the treatment of PTSD [12].
• A case is reported in which the MAO inhibitor isocarboxazid was successfully used to treat both depression and associated trichotillomania [13].
• Triiodothyronine (T3)-induced hyperthyroidism did not affect MAO activity [14].
• MAO inhibitors in panic disorder: clinical effects of treatment with brofaromine. A double blind placebo controlled study [15].

Biological context of MAO

• It is primarily metabolized by oxidative deamination by MAO and possesses an extremely rapid turnover and half-life [16].
• The Norrie disease and MAO genes are tandemly arranged in the p11.4-p11.3 region of the human X chromosome in the order tel-MAOA-MAOB-NDP-cent [17].
• When the complex [4-CH(3)-C(6)H(4)C(NTMS)(2)](2)ZrMe(2) (9) was activated with MAO, it was found to be a good catalyst for the polymerization of propylene, at atmospheric pressure, producing an oily polymer resembling an atactic polypropylene [18].
• DNA was genotyped for functional variants of the COMT and MAO genes, and allele inheritance was examined using the Transmission Disequilibrium Test (TDT) and Haplotype-based Haplotype Relative Risk (HHRR) test [19].
• However, DA-induced dysregulation of calcium homeostasis seems to be more specifically mediated by DA metabolism by MAO [20].

Anatomical context of MAO

• In glial cells, MAO may also play a role to regulate concentration of telemethylhistamine and trace amines [10].
• MAO is present in astroglial cells, in which monoamines released in extracellular space may be degraded [10].
• Monoamine oxidase (EC 1.4.3.4; MAO) is the primary enzyme responsible for the intraneuronal degradation of biogenic amines in the central nervous system [21].
• The type of MAO in the endothelial cells was found to be exclusively of the A type [22].
• Administration of different steroid hormones in vivo has distinct and specific effects on the MAO activity of the adrenal medulla [22].

Associations of MAO with other chemical compounds

• MAO A-3C9 appears to have a lower affinity for purified MAO A than the other three antibodies and does not immunoprecipitate either MAO A or MAO B from human platelets or from Triton X-100 extracts of human placental and liver mitochondria [21].
• Furthermore, pretreatment with deprenyl (MAO-inhibitor) or alpha-methyl-L-p-tyrosine (TH-inhibitor) also suppressed dieldrin-induced ROS generation and DNA fragmentation [23].
• Platelet MAO activity and platelet serotonin uptake were determined in 20 agoraphobic and 16 neurotic depressive out-patients, and 19 healthy volunteers [24].
• The antidepressant drug clorgyline, a monoamine oxidase inhibitor (MAOI) that selectively inhibits MAO type A was administered chronically to Syrian hamsters [25].
• The inhibiton of type A and B MAO in rat forebrain crude membrane preparation by MD780515, (3-(4-[(3-cyanophenyl)methoxy]phenyl)-5-(methoxymethyl)-2-oxazolidinone-Centre de Recherche Delalande, France) has been investigated in vitro with 5-hydroxytryptamine and beta-phenylethylamine as substrates [26].

Gene context of MAO

• We describe here four new monoclonal antibodies (designated MAO A-3C9, A-4F10, A-7B10, and A-7E10) which were elicited to highly purified MAO A from human placenta and which, in the presence of antimouse IgG and Staphylococcus aureus, immunoprecipitate greater than 90% of the catalytically active purified MAO A [21].
• During this time, the MAO-B activity increased from approximately 40 to approximately 60% of the total MAO activity [27].
• This study did not indicate any involvement of FMO3 or MAO in the in vitro metabolism of Lu 25-109 in human liver microsomes [28].
• These results are discussed in terms of several mechanisms proposed for MAO catalysis and with previous structure-activity studies published with bovine liver MAO B [Walker, M. C., and Edmondson, D. E. (1994) Biochemistry 33, 7088-7098] [29].
• Acutely, SMS 201-995 decreased acid secretion and restored the BAO/MAO ratio to normal in eight of eight patients [30].

Analytical, diagnostic and therapeutic context of MAO

• The neurogenic pathway is activated during reperfusion after 15-minute MAO, because sustained MAO failed to produce cardioprotection [2].
• The mean platelet MAO activity for the chronic schizophrenic patients was significantly lower than the mean in either control group [31].
• All MAO B-containing extracts, regardless of tissue source, inhibited immunoprecipitation of [3H]pargyline-labeled human platelet MAO, and the shapes of the inhibition curves were identical [32].
• CONCLUSIONS: Elevations in BDNF protein in brain are consistent with the greater treatment efficacy of ECS and MAO inhibitors in drug-resistant major depressive disorder and may be predictive for the antidepressant action of the more highly efficacious interventions [33].
• Monoamine oxidase content in extracts of human blood platelets was determined independently of MAO activity measurements with a recently developed monoclonal antibody against human platelet monoamine oxidase (MAO B) in a competitive radioimmunoassay [34].

References