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Influence of oxidative stress on disease development

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Author(s): Božić Tatjana | Stevanović Jelka | Borozan Sunčica | Jović Slavoljub | Dimitrijević Blagoje | Ignjatović Igor

Journal: Veterinarski Glasnik
ISSN 0350-2457

Volume: 67;
Issue: 1-2;
Start page: 75;
Date: 2013;
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Keywords: oxidative stress | atherosclerosis | hypertension | Diabetes mellitus | heart failure | stroke | rheumatoid arthritis

ABSTRACT
There is ever increasing data indicating the vmast contribution of oxidative stress to the pathogenesis of numerous diseases (atherosclerosis, hypertension, heart failure, diabetes mellitus, stroke, rheumatoid arthritis, and others). Thus, in the pathogenesis of atherosclerosis the primary role is held by reactive oxygen species that are synthetized by endothelial cells of arterial blood vessels, leukocytes and macrophages. Furthermore, native particles of lipoproteins of small density become atherogenic through oxidation caused by reactive oxygen species. The oxidation of small-density lipoproteins stimulates the inflammatory process, and it in turn steps up adhesion and the inflow of monocytes and affects the synthesis and release of numerous proinflammatory cytokines involved in the further course of the process. One of the reasons for the development of arterial hypertension is the simultaneous activation of NAD(P)H oxidase and 12/15-lipoxygenase, since it results in the stepped up production of reactive oxygen species. These stimulate the production of matrix metalloproteinase 2, which lead to vascular remodelling and to increased apoptosis of heart muscle cells. Stepped up apoptosis is linked with myocardial infarction, cardiomyopathies and the development of heart failure. The sensitivity of β-cells of the endocrine part of the pancreas to reactive oxygen species favor the naturally low concentrations of the collectors of free radicals in them, as well as an increase in the concentration of proinflammatory cytokines, glucosis and lipids that induce a reduction in the mass and function of β-cells. Hyperglycemia in diabetes mellitus causes tissue damage through non-enzyme glycosylation of intracellular and extracellular proteins, which results in: reduced enzyme activity, damaged nucleic acid, disrupted natural decomposition of proteins, and activation of cytotoxic pathways. These processes are the basis of the pathogenesis of numerous complications of diabetes mellitus. Since inducible nitrogen-oxide synthesis launches processes that stimulate apoptosis of cerebral endothelial cells, and superoxide-anion radicals, hypochloric acid and hydrogen peroxide damage the parenchyma of an ischemic brain and biomacromolecules (causing lipid peroxidation, oxidation of proteins and deoxyribonucleic acid), brain damage occurs during cerebral ischemia and reperfusion. [Projekat Ministarstva nauke Republike Srbije, br. 173034, br. 175061 i br. 31085]
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