D-Amphetamine-Induced Hydrogen Peroxide Production in Skeletal Muscle is Modulated by Monoamine Oxidase Inhibition

Abstract

The aim of this paper was to study the influence of d-amphetamine administration as a sympathomimetic drug on the synthesis of hydrogen peroxide (H2O2) in mouse soleus muscle and to investigate the modulating effects of pargyline, an inhibitor of monoamine oxidase (MAO) in this context. Charles River mice were assigned to four groups: Control, d-amphetamine treated, pargyline treated, and amphetamine + pargyline treated. Their soleus muscles were removed 0, 15, 30, 60, and 120 min after treatment. The amount of hydrogen peroxide formation within the muscles was estimated using an indirect method. The control data showed a continuous production of hydrogen peroxidase. Pargyline administration lead to an initial increase of H2O2 production that later faded below control levels. Administration of amphetamine finally stimulated H2O2 production much above control levels. When combining amphetamine and pargyline treatment, H2O2 production was accelerated in the initial phase but dropped to control levels at 30 min. It is concluded that in skeletal muscle MAO is an important source of hydrogen peroxide production triggered by amphetamine administration and that this tissue plays a hitherto not described role in oxidizing circulating biogenic monoamines.

Action mechanism and cardiovascular effect of anthocyanins: a systematic review of animal and human studies

“…These factors increase the likelihood of the onset of cardiovascular disease and they are related with increased oxidative stress in the body [31–35], which could increase the macromolecules damage. Accordingly, clinical and experimental studies have shown that oxidative stress is associated with the pathogenesis of cardiovascular processes, with high production of ROS in relation to antioxidant factors, which exhibit low or unchanged activity [36–39]. In addition, the heart is an organ with the lower concentrations of antioxidant in the body, which leads to increased ROS production, so it is most prone to tissue and cells damage, mainly in macromolecules, as DNA, proteins and cell lipids [36, 37, 40].…”

Contribution of Catecholamine Reactive Intermediates and Oxidative Stress to the Pathologic Features of Heart Diseases

“…The highly reactive HO [183] causes oxidative stress-related damage, especially in organs with very low antioxidant defenses such as the heart [395,396]. In fact, MAO inhibitors have been found to decrease the incidence and severity of myocardial lesions following catecholamine administration [397,398].…”

Adrenaline and Noradrenaline: Partners and Actors in the Same Play"

“…Dopamine, tyramine, and tryptamine are oxidized with equal affinity by MAO-A and MAO-B (Glover et al, 1977). Pargyline inhibits both MAO-A and MAO-B (Blaha et al, 1996, Carvalho et al, 2001, Carmo et al, 2003, Duarte et al, 2004. MAO-A appears to be the main enzyme in the metabolism of 5-HT and NA, while the location of MAO-B, abundant in serotonergic neurons, remains under debate (Abell and Kwan, 2001).…”

“…Of relevance, the oxidative deamination of catecholamines by MAO leads to another relevant product, hydrogen peroxide (H 2 O 2 ) which subsequently may be converted into the highly reactive hydroxyl radical (HO • ) (Valko et al, 2007), that may cause oxidative stressrelated damage (Carvalho et al, 2001, Duarte et al, 2004, Vaarmann et al, 2010, Costa et al, 2011.…”