A ratiometric electrochemical sensor for selectively monitoring monoamine oxidase A in the live brain

2021 ◽  
Author(s):  
Chuanping Zhang ◽  
Chenxiao Tang ◽  
Yuxiao Mei ◽  
Limin Zhang ◽  
Anwei Zhu ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Electrochemical Sensor ◽  
Electrochemical Method ◽  
Monoamine Oxidase A ◽  
Mao A ◽  
Live Mouse

Herein, an electrochemical method for selectively sensing and accurately quantifying of monoamine oxidase A (MAO-A) in cortex and thalamus of live mouse brains was reported. Using this tool, it was...

Are Coumarin Derivatives The New Keys in Depression Treatment? In silico Key-lock Fitting Analysis of Coumarin Derivatives with Monoamine Oxidase-A

2020 ◽  
Vol 7 ◽  
Author(s):  
Dilara Karaman ◽  
Kemal YELEKCI ◽  
Serkan ALTUNTAS
Keyword(s):  
Monoamine Oxidase ◽  
Protein Interactions ◽  
In Silico ◽  
Monoamine Oxidase A ◽  
Coumarin Derivatives ◽  
Discovery Studio ◽  
Mao B ◽  
Drug Candidates ◽  
Mao A ◽  
Molecular Modeling Studies

The research of ligand-protein interactions with in silico molecular modeling studies on the atomic level gives an opportunity to be understood the pharmacokinetic metabolism of anti-depressant drug candidates. Monoamine oxidase (MAO) enzymes are important targets for the treatment of depressive disorder. MAOs have two isoforms as MAO-A and MAO-B being responsible for catalyzing of neurological amines. In this study a new series of coumarin derivatives were designed for selective and reversible inhibition of MAO-A enzyme. 3rd, 5th and 7th positions were selected to be placed of five different side groups. Docking procedures of each ligand in M series of these novel 125 compounds were executed with 10 runs by using AutoDock4.2 software. Docking results were analyzed via Discovery Studio 3.1 (Biovia Inc.). The most promising compounds were M118 and M123 according to selectivity index, SI (MAO-B/MAO-A)=180 fold and 209 fold and Ki values 7.25 nM and 12.01 nM, respectively. Overall, the current study provided significant knowledge for the development of new anti-depressant drugs.

Polymorphisms of the serotonin transporter and Monoamine Oxidase A gene in patients with metastatic midgut carcinoid tumors

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 4557-4557
Author(s):  
A. van der Horst-Schrivers ◽  
E. de Vries ◽  
P. Willemse ◽  
I. Kema ◽  
T. Links ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Serotonin Transporter ◽  
Promoter Region ◽  
Carcinoid Tumors ◽  
Monoamine Oxidase A ◽  
Independent Effect ◽  
Clinical Effects ◽  
Cox Regression Analysis ◽  
Midgut Carcinoid ◽  
Mao A

4557 Background: In patients with metastatic midgut carcinoid tumors increased serotonin secretion is related to the carcinoid syndrome and mortality. Free serotonin is taken up via the serotonin transporter (5-HTT) in the liver and the lung and metabolized to 5- hydroxyindolacetic acid (5-HIAA) by Monoamine Oxidase A (MAO-A). The 5-HTT gene has a functional polymorphism in the promoter region (5-HTTPLR), with a short (S, less active) and long (L) allele and a polymorphic region in the second intron with variable number tandem repeats (VNTR-2). The MAO-A gene contains a length polymorphism in its promoter region (MAOA-LPR). To determine the clinical effects of the serotonin metabolizing capacity of individual patients, the association between different genotypes and symptoms (flushes and diarrhea) and survival was studied. Methods: 107 patients with metastatic midgut carcinoid tumors were genotyped for 5-HTTPLR, VNTR-2 and MAO-A-LPR. Differences were tested using Chi-square test and survival according to genotypes was analyzed using Kaplan Meier survival curves and tested with a log rank test. The independent effect of genotypes on survival was studied with multivariate Cox regression analysis with adjustments for the urinary 5-HIAA level, age at presentation and the presence of liver metastases. Results: The various genotypic variants were not related to flushes or diarrhea. Patients with the SS variant of 5-HTTLPR had a shorter median survival (45 months, 95% Confidence Interval (CI) 0.50–90) compared to patients with the LS (113 months, 95% CI 53–172) and the LL variant (90 months, 95% CI 64–115) (P=0.02). After adjustment, survival in patients with the SS variant remained worse with an odds ratio of 0.43 (95% CI 0.23–0.83; P=0.009) and 0.63 (95% CI 0.33–1.11; P=0.1) compared to patients with the LS and the LL variant respectively. Survival was not influenced by the VNTR-2 or MAOA-LPR. Conclusions: The SS genotype of the 5-HTTLPR is independently associated with a worse survival in patients with metastatic midgut carcinoid tumors. No significant financial relationships to disclose.

scholarly journals Involvement of Monoamine Oxidase a (MAO-A) in mitochondrial fission and autophagy during aging

2013 ◽  
Vol 34 (suppl 1) ◽  
pp. P1856-P1856 ◽  
Author(s):  
F. Vigneron ◽  
C. Guilbeau-Frugier ◽  
A. Parini ◽  
J. Mialet-Perez
Keyword(s):  
Monoamine Oxidase ◽  
Mitochondrial Fission ◽  
Monoamine Oxidase A ◽  
Mao A

Brain monoamine oxidase A in hyperammonemia is regulated by NMDA receptors

2009 ◽  
Vol 4 (3) ◽  
pp. 321-326
Author(s):  
Elena Kosenko ◽  
Yury Kaminsky
Keyword(s):  
Oxidative Stress ◽  
Nmda Receptor ◽  
Monoamine Oxidase ◽  
Nmda Receptors ◽  
Monoamine Oxidase A ◽  
Mk 801 ◽  
Mao A ◽  
Vitro Effect

AbstractMitochondrial enzyme monoamine oxidase A (MAO-A) generates hydrogen peroxide (H2O2) and is up-regulated by Ca2+ and presumably by ammonia. We hypothesized that MAO-A may be under the control of NMDA receptors in hyperammonemia. In this work, the in vivo effects of single dosing with ammonia and NMDA receptor antagonist MK-801 and the in vitro effect of Ca2+ on MAO-A activity in isolated rat brain mitochondria were studied employing enzymatic procedure. Intraperitoneal injection of rats with ammonia led to an increase in MAO-A activity in mitochondria indicating excessive H2O2 generation. Calcium added to isolated mitochondria stimulated MAO-A activity by as much as 84%. MK-801 prevented the in vivo effect of ammonia, implying that MAO-A activation in hyperammonemia is mediated by NMDA receptors. These data support the conclusion that brain mitochondrial MAO-A is regulated by the function of NMDA receptors. The enzyme can contribute to the oxidative stress associated with hyperammonemic conditions such as encephalopathy and Alzheimer’s disease. The attenuation of the oxidative stress highlights MAO-A inactivation and NMDA receptor antagonists as sources of novel avenues in the treatment of mental disorders.

scholarly journals Monoamine oxidase A (MAO A) inhibitors decrease glioma progression

Oncotarget ◽  
2016 ◽  
Vol 7 (12) ◽  
pp. 13842-13853 ◽  
Author(s):  
Swati Kushal ◽  
Weijun Wang ◽  
Vijaya Pooja Vaikari ◽  
Rajesh Kota ◽  
Kevin Chen ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Monoamine Oxidase A ◽  
Mao A ◽  
Glioma Progression

Monoamine oxidase-A targeting probe for prostate cancer imaging and inhibition of metastasis

2019 ◽  
Vol 55 (88) ◽  
pp. 13267-13270 ◽  
Author(s):  
Won Young Kim ◽  
Miae Won ◽  
Abbas Salimi ◽  
Amit Sharma ◽  
Jong Hyeon Lim ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Monoamine Oxidase ◽  
Cancer Imaging ◽  
Monoamine Oxidase A ◽  
Mitochondrial Enzyme ◽  
Mao A ◽  
Enzyme Monoamine Oxidase

Mitochondrial enzyme monoamine oxidase (MAO-A) is known to be overexpressed in prostate cancer (PCa) cells.

Abstract 421: Norepinephrine Catabolism Drives Cardiac Fibroblast Activation via Monoamine Oxidase Activity and Rage/β-adrenergic Signaling

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Blake Monroe ◽  
Ethan J Anderson
Keyword(s):  
Monoamine Oxidase ◽  
Cardiac Fibrosis ◽  
Cardiac Fibroblasts ◽  
Advanced Glycation Endproducts ◽  
Cardiac Fibroblast ◽  
Monoamine Oxidase A ◽  
Matrix Remodeling ◽  
Mao A ◽  
Canonical Pathways ◽  
Accelerated Proliferation

The mitochondrial enzyme monoamine oxidase A (MAO-A) plays an increasingly appreciated role in cardiac remodeling induced by diabetes and ischemic injury. Oxidative deamination of norepinephrine (NE) by MAO-A generates 3,4-dihydroxyphenylglycolaldehyde (DOPEGAL) and H 2 O 2 . Isolation and quantification of catechol-modified proteins from cardiac fibroblast lysate using an aminophenylboronic acid resin showed an MAO-dependent accumulation of catechol adducts in NE-treated cells (P<0.05). Our lab has previously observed increased expression and activity of MAO in myocardium of diabetes patients compared with age-matched nondiabetic patients. Moreover, preliminary data suggest that catecholaldehydes and other biogenic aldehydes might contribute to the pathogenesis of cardiac fibrosis in diabetic cardiomyopathy via pro-fibrotic signaling mechanisms. We hypothesize that NE activates fibroblasts by both canonical pathways (i.e, adrenergic receptors) and by monoamine oxidase-mediated catabolism and activation of the receptor for advanced glycation endproducts (RAGE). Treatment of cardiac fibroblasts with NE (1 μM) resulted in accelerated proliferation, enhanced collagen I & III secretion, robust increases in mitochondrial and total cellular ROS, and upregulated pro-fibrotic gene expression. These effects were abrogated by co-administration of RAGE antagonist FPS-ZM1, MAO inhibitors, β-blocker propranolol, and the aldehyde scavenger carnosine (P<0.05). These findings suggest that NE (and other catecholamines) may influence extracellular matrix remodeling via multiple pathways, including adrenergic and also RAGE, via MAO-mediated catabolism.

The interleukin-6, serotonin transporter, and monoamine oxidase A genes and endurance performance during the South African Ironman Triathlon

2009 ◽  
Vol 34 (5) ◽  
pp. 858-865 ◽  
Author(s):  
Liesl de Milander ◽  
Dan J. Stein ◽  
Malcolm Collins
Keyword(s):  
Monoamine Oxidase ◽  
South African ◽  
Gene Polymorphisms ◽  
Endurance Performance ◽  
Monoamine Oxidase A ◽  
Endurance Capacity ◽  
Functional Polymorphisms ◽  
Central Governor ◽  
Mao A ◽  
Ironman Triathlon

Previous studies have identified an association of genetic variants believed to alter physiological and biochemical processes locally within the skeletal muscle and therefore performance in the Ironman triathlon. There is growing evidence that the serotonergic system and circulating interleukin (IL)-6 levels are also involved in mediating endurance capacity. Investigators have demonstrated that recombinant human IL-6 administration and serotonergic neurotransmission manipulation, with 5-hydroxytryptamine transporter (5-HTT) and monoamine oxidase A (MAO-A) inhibitors, prior to exercise, can alter running performance, consistent with a central governor hypothesis. The aim of this study was to investigate possible associations of functional polymorphisms within the IL-6 , 5-HTT , and MAO-A genes with endurance performance of Ironman triathletes. Four hundred sixty-eight male Caucasian triathletes who completed the 2000 and (or) 2001 South African Ironman Triathlon and 200 healthy Caucasian male controls were genotyped for the –174 IL-6 G/C, 5-HTT 40 base pair (bp) insertion–deletion and 30 bp variable number of tandem repeats (VNTR) MAO-A gene polymorphisms. There were no significant differences in the relative genotype distributions within the IL-6 (p = 0.636), 5-HTT (p = 0.659), and MOA-A (p = 0.227) polymorphisms when the fastest-fnishing, middle-finishing, and slowest-finishing triathletes, as well as the control groups, were compared. There were no direct associations between the IL-6 –174 G/C, 5-HTT 44 bp insertion–deletion, and MAO-A 30 bp VNTR gene polymorphisms and endurance performance in the 2000 and (or) 2001 South African Ironman Triathlons. The neurogenetic basis of the central governor requires further investigation.

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