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Monoamine oxidases are novel sources of cardiovascular oxidative stress in experimental diabetes
Adrian Sturza1,2, Oana M Duicu1,2, Adrian Vaduva3
1a Department of Pathophysiology, Faculty of Medicine, "Victor Babeş" University of Medicine and Pharmacy, 14, Tudor Vladimirescu st., 300173 Timişoara, Romania.
Abstract:
Diabetes mellitus (DM) is widely recognized as the most severe metabolic disease associated with increased cardiovascular morbidity and mortality. The generation of reactive oxygen species (ROS) is a major event causally linked to the development of cardiovascular complications throughout the evolution of DM. Recently, monoamine oxidases (MAOs) at the outer mitochondrial membrane, with 2 isoforms, MAO-A and MAO-B, have emerged as novel sources of constant hydrogen peroxide (H2O2) production in the cardiovascular system via the oxidative deamination of biogenic amines and neurotransmitters. Whether MAOs are mediators of endothelial dysfunction in DM is unknown, and so we studied this in a streptozotocin-induced rat model of diabetes. MAO expression (mRNA and protein) was increased in both arterial samples and hearts isolated from the diabetic animals. Also, H2O2 production (ferrous oxidation - xylenol orange assay) in aortic samples was significantly increased, together with an impairment of endothelium-dependent relaxation (organ-bath studies). MAO inhibitors (clorgyline and selegiline) attenuated ROS production by 50% and partially normalized the endothelium-dependent relaxation in diseased vessels. In conclusion, MAOs, in particular the MAO-B isoform, are induced in aortas and hearts in the streptozotocin-induced diabetic rat model and contribute, via the generation of H2O2, to the endothelial dysfunction associated with experimental diabetes.
Insights
Monoamine oxidases (MAOs) contribute to cardiovascular complications in diabetes by increasing hydrogen peroxide (H2O2) production, leading to endothelial dysfunction. Inhibiting MAOs partially restored normal blood vessel function in diabetic rats.
Area of Science:
- Biochemistry
- Cardiovascular Biology
- Metabolic Diseases
Background:
- Diabetes mellitus (DM) significantly increases cardiovascular morbidity and mortality.
- Reactive oxygen species (ROS) generation is a key factor in DM-related cardiovascular complications.
- Monoamine oxidases (MAOs), particularly MAO-A and MAO-B, are identified as novel sources of hydrogen peroxide (H2O2) in the cardiovascular system.
Purpose of the Study:
- To investigate the role of MAOs in mediating endothelial dysfunction in a rat model of diabetes.
- To determine if MAO expression and activity are altered in diabetic cardiovascular tissues.
- To assess the therapeutic potential of MAO inhibitors in mitigating diabetes-induced endothelial dysfunction.
Main Methods:
- Induction of diabetes in rats using streptozotocin.
- Quantification of MAO expression (mRNA and protein) in aortic and heart samples.
- Measurement of H2O2 production in aortic tissues using the ferrous oxidation - xylenol orange assay.
- Assessment of endothelium-dependent relaxation using organ-bath studies.
- Administration of MAO inhibitors (clorgyline and selegiline).
Main Results:
- Increased MAO expression and elevated H2O2 production were observed in the aortas and hearts of diabetic rats.
- Diabetic rats exhibited impaired endothelium-dependent relaxation.
- Treatment with MAO inhibitors significantly reduced ROS production and partially improved endothelial function.
Conclusions:
- MAO-A and MAO-B isoforms are upregulated in the cardiovascular system of diabetic rats.
- MAO-mediated H2O2 generation contributes to endothelial dysfunction in experimental diabetes.
- MAO inhibition represents a potential therapeutic strategy for managing cardiovascular complications in diabetes.
