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- W2980335077 abstract "In recent years, it has become apparent that autoimmune mechanisms play a leading role in the development of insulin-dependent diabetes mellitus (IDDM). According to modern concepts, IDDM is a classic organ-specific autoimmune disease in which -cells are destroyed by mechanisms mediated by T-lymphocytes and circulating autoantibodies. However, there is experimental evidence that the primary mechanism of damage to the p-cell is the action of cytokines. Thus, the destruction of -cells occurs in two phases: the first - independent of lymphocytes, the initial, the second - mediated by the action of T-lymphocytes. According to the Copenhagen model of the pathogenesis of IDDM, environmental and internal factors (viruses, chemicals, food factors, interleukin-1) trigger the activation of free radical oxidation in -cells. Under the influence of free radicals (O2-, NO), p-cell proteins change their natural properties (denature) and become antigens for their own immune system. The increased sensitivity of the -cell to the action of free radicals is due to the fact that it reduces the activity of antioxidant defense systems (superoxide dismutase, glutathione peroxidase, catalase). In other words, -cells in IDDM die because they are b-cells. Toxic free radicals of oxygen (O2-) and nitric oxide (NO) cause disturbances in the DNA structure of insulin-producing cells, stimulate the pathological activation of poly (ADP-ribose) synthetase, responsible for DNA replication, which leads to increased utilization of NAD + with subsequent depletion of its reserves in the cell: this causes a decrease in the synthesis of proteins, including proinsulin, and the subsequent death of the -cell." @default.
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- W2980335077 date "1996-12-15" @default.
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- W2980335077 title "Nicotinamide in the treatment of insulin-dependent diabetes mellitus at the debut of the disease" @default.
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- W2980335077 doi "https://doi.org/10.14341/probl12057" @default.
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