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Role of Oxidative Stress in the Genesis of Atherosclerosis and Diabetes Mellitus: A Personal Look Back on 50 Years of Research

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We have provided an overview, based on the literature and our data. In accordance with the theory of D. Harman free radical processes cause damages that can accumulate and contribute to aging of the organism. Atherosclerosis and diabetes are developing for a long time so they are manifested predominantly in old age. We found an increase in the level of free radical peroxidation products and decrease in the activity of antioxidant enzymes in the tissues of animals with experimental atherosclerosis. Similar changes were found in the blood of patients with atherosclerosis and aortic autopsy material with atherosclerotic lesions. Thus, it was revealed that oxidative stress occured under atherosclerosis, and the arteriosclerosis to "Free Radical Pathologies" was attributed. Later it was discovered by different authors that oxidized Low Density Lipoproteins (LDL) and malonyldialdehyde- modified LDL accumulated during atherogenesis, causing damages of vascular wall. Under diabetic hyperglycemia glucose co-oxidized during free radical lipoperoxidation. This process promoted the transformation of oxidative stress to carbonyl stress with accumulation of biologically active dicarbonyls, including glyoxal and methylglyoxal. We show that the glyoxal-modified LDL were captured by cultured macrophages with a higher efficiency than the MDA-modified LDL. This could facilitate the more rapid development of lipoidosis in the vessel wall (due to the formation of foam cells) and manifestation of atherosclerosis under diabetes. We found that in patients with diabetes there was a sharp decrease in the activity of antioxidant enzymes as a result of the modification of the active center under development of carbonyl stress. We expressed a hypothesis about a common molecular mechanism of vascular wall damages under atherosclerosis and diabetes.
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Keywords: Atherosclerosis; carbonyl stress; diabetes; free radical peroxidation; oxidative stress; oxidized LDL; reactive oxygen species

Document Type: Research Article

Publication date: February 1, 2017

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  • Current Aging Science publishes frontier review and experimental articles in all areas of aging and age-related research that may influence longevity. This multidisciplinary journal will help in understanding the biology and mechanism of aging, genetics, pathogenesis, intervention of normal aging process and preventive strategies of age-related disorders. The journal publishes objective reviews written by experts and leaders actively engaged in research using cellular, clinical, molecular, and animal models, including lower organism models (e.g., yeast, Caenorhabditis elegans and Drosophila). In addition to the affect of aging on integrated systems, the journal also covers original articles on recent research in fast emerging areas of adults stem cells, brain imaging, calorie restriction, immunosenescence, molecular diagnostics, pharmacology and clinical aspects of aging. Manuscripts are encouraged that relate to developmental programming of aging and the synergistic mechanism of aging with cardiovascular diseases, obesity and neurodegenerative disorders.

    Book reviews, meeting reports and letters-to-the-editor and drug clinical trial studies are also published. The journal is essential reading for researchers, educators and physicians with interest in aging, age-related dementia and Alzheimer's disease and longevity. Current Aging Science provides a comprehensive coverage of the current state of aging research for gerontologists, neuroscientists, clinicians, health science planners, granting agencies and pharmaceutical scientists.

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