Monoamine oxidase-A, serotonin and norepinephrine: synergistic players in cardiac physiology and pathology

Mialet‐Perez, Jeanne; Santin, Yohan; Parini, Angelo

doi:10.1007/s00702-018-1908-y

Cited by 40 publications

(30 citation statements)

References 57 publications

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“…Studies have shown that increased serotonin uptake and oxidative stress could be the cause of platelet activation. Increased serotonin metabolism and subsequent MAO activity induce oxidative stress, and consequently, oxidative stress may activate platelet activation (Bianchi, Pimentel, Murphy, Colucci, & Parini, ; Mialet‐Perez, Santin, & Parini, ; Sugiura et al, ). Our result showed a significant elevation of ROS in patient with PD and reduction in TAC, so it can affect the RBC membrane and causes significant alterations of RDW and MCHC (Mehrpour et al, ).…”

Section: Discussionmentioning

confidence: 99%

Changes in mean platelet volume and hematologic indices in patients with panic disorder due to oxidative stress

Hamzekolaei¹,

Jafarisani

Farajzadeh

et al. 2020

Brain and Behavior

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Objective: Cardiovascular disorders are common in patients with panic disorder (PD), usually mediated by platelets. The present study was conducted to evaluate oxidative stress conditions and complete analysis of blood cells in patients with PD. Setting and Sample Population:Sixty healthy individuals and 60 patients were included in the study. Whole blood and serum samples were obtained from patients and controls. Materials & Method:Hematological studies, including blood cells count, hemoglobin, and hematocrit, were carried out on whole blood samples. In addition, oxidative stress indices including total antioxidant capacity, free oxygen species, and malondialdehyde concentration were measured in serum samples. Results:Results showed that patients with PD had a significant increase in mean platelet volume index (MPV), platelet distribution width (PDW), red blood cell distribution width (RDW), and mean corpuscular hemoglobin concentration (MCHC) compared with healthy subjects (p < .05). Also, oxidative stress indices were significantly elevated in patients with PD compared with control group (p < .05). Conclusion:Elevated MPV is a hematologic indicator for patients with PD. This disorder may be caused by impaired serotonin metabolism, resulting in increased oxidative stress, as well as in platelet serotonin transporters. Regarding elevated oxidative stress, the risk of cardiovascular complications is high in patients with PD. K E Y W O R D S MCHC, MPV, oxidative stress, panic disorder, RDW How to cite this article: Naghipour Hamzekolaei M, Jafarisani M, Farajzadeh A, et al. Changes in mean platelet volume and hematologic indices in patients with panic disorder due to oxidative stress. Brain Behav. 2020;10:e01569. https://doi.

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Section: Discussionmentioning

confidence: 99%

Changes in mean platelet volume and hematologic indices in patients with panic disorder due to oxidative stress

Hamzekolaei¹,

Jafarisani

Farajzadeh

et al. 2020

Brain and Behavior

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“…Since high levels of ROS are generated during the development of ischemia/reperfusion injury as well as upon the oxidation of catecholamines by both enzymatic and non-enzymatic mechanism, it has been argued that ventricular arrhythmias are induced by oxidative stress in the myocardium [ 5 , 6 , 14 , 44 , 45 , 46 , 47 , 48 ]. This concept is consistent with observations [ 15 ] that treatment of animals with well-known antioxidants such as vitamin E and N -acetyl-cysteine prevented the epinephrine-induced different types of arrhythmias as well as increased the levels of plasma malondialdehyde, an index of oxidative stress ( Table 3 ).…”

Section: Oxidative Stress As a Factor For Increasing The Risk Of Amentioning

confidence: 99%

“…Thus, the beneficial effects of angiotensin converting enzyme inhibitors as well as angiotensin II receptor blockers in attenuating ventricular arrhythmias in ischemic heart disease appears to be due to reduction in the degree of oxidative stress. Likewise, the prevention of ventricular arrhythmias due to coronary artery occlusion by a 5-hydroxytryptamine (5-HT) receptor inhibitor, sarpogrelate [ 17 , 75 ], may also be attributed to its effect on oxidative stress because the circulating level of serotonin (5-HT) was increased in myocardial infarction [ 76 ] and serotonin has been shown to generate oxyradicals upon oxidation due to monoamine oxidase [ 48 ].…”

Section: Oxidative Stress As a Factor For Increasing The Risk Of Amentioning

confidence: 99%

Role of Oxidative Stress in the Genesis of Ventricular Arrhythmias

Adameová

Shah

Dhalla

2020

IJMS

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Ventricular arrhythmias, mainly lethal arrhythmias, such as ventricular tachycardia and fibrillation, may lead to sudden cardiac death. These are triggered as a result of cardiac injury due to chronic ischemia, acute myocardial infarction and various stressful conditions associated with increased levels of circulating catecholamines and angiotensin II. Several mechanisms have been proposed to underlie electrical instability of the heart promoting ventricular arrhythmias; however, oxidative stress which adversely affects ion homeostasis due to changes in the ion channel structure and function, seems to play a critical role in eliciting different types of ventricular arrhythmias. Prevention or mitigation of the severity of ventricular arrhythmias due to antioxidants has been indicated as the fundamental contribution in the field of preventive cardiology; however, novel interventions have to be developed for greater effectiveness and specificity in attenuating the adverse effects of oxidative stress. In this review, we have attempted to discuss proarrhythmic effects of oxidative stress differing in time and concentration dependence and highlight a molecular and cellular concept how it alters cardiac cell automaticity and conduction velocity sensitizing the probability of ventricular arrhythmias with resultant sudden cardiac death due to ischemic heart disease and other stressful situations. It is concluded that pharmacological approaches targeting multiple mechanisms besides oxidative stress might be more effective in the treatment of ventricular arrhythmias than current antiarrhythmic therapy.

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“…2 A depletion of serotonin in the CNS is responsible for disorders such as obsessive–compulsive disorders, depression, and anxiety, 3 while its role in mediating inflammation and immunity responses 4 as well as its relevance for cardiac physiology and pathology has also been proposed. 5 Increasing serotonin levels is an important strategy in the pharmacological treatment of depression, and typically, the levels are increased by inhibiting the serotonin transporter or by inhibiting monoamine oxidase A (MAO A), an enzyme that breaks down serotonin. 6 MAOs are flavoenzymes that catalyze the oxidative deamination of biogenic amines, producing aldehyde and hydrogen peroxide.…”

Section: Introductionmentioning

confidence: 99%

How Monoamine Oxidase A Decomposes Serotonin: An Empirical Valence Bond Simulation of the Reactive Step

et al. 2020

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The enzyme-catalyzed degradation of the biogenic amine serotonin is an essential regulatory mechanism of its level in the human organism. In particular, monoamine oxidase A (MAO A) is an important flavoenzyme involved in the metabolism of monoamine neurotransmitters. Despite extensive research efforts, neither the catalytic nor the inhibition mechanisms of MAO enzymes are currently fully understood. In this article, we present the quantum mechanics/molecular mechanics simulation of the rate-limiting step for the serotonin decomposition, which consists of hydride transfer from the serotonin methylene group to the N5 atom of the flavin moiety. Free-energy profiles of the reaction were computed by the empirical valence bond method. Apart from the enzymatic environment, the reference reaction in the gas phase was also simulated, facilitating the estimation of the catalytic effect of the enzyme. The calculated barrier for the enzyme-catalyzed reaction of 14.82 ± 0.81 kcal mol –1 is in good agreement with the experimental value of 16.0 kcal mol –1 , which provides strong evidence for the validity of the proposed hydride-transfer mechanism. Together with additional experimental and computational work, the results presented herein contribute to a deeper understanding of the catalytic mechanism of MAO A and flavoenzymes in general, and in the long run, they should pave the way toward applications in neuropsychiatry.

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Monoamine oxidase-A, serotonin and norepinephrine: synergistic players in cardiac physiology and pathology

Cited by 40 publications

References 57 publications

Changes in mean platelet volume and hematologic indices in patients with panic disorder due to oxidative stress

Changes in mean platelet volume and hematologic indices in patients with panic disorder due to oxidative stress

Role of Oxidative Stress in the Genesis of Ventricular Arrhythmias

How Monoamine Oxidase A Decomposes Serotonin: An Empirical Valence Bond Simulation of the Reactive Step

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