A radical is any molecule that contains one or more unpaired electrons.Radicals are normally generated in many metabolic pathways.Some of these radicals can exist in free form and subsequentky interact with various tissue components resulting in dysfunction. The potential role oxygen- and xenobiotic- derived free radical in the pathology of several human diseases stimulated extensive research linking the toxity of numerous xenobiotics and disease processes to a free radical machanism.
L-ascorbic acid is one of the basic vitamins, necessary to the normal growth and behaviour of organisms. The primary of this review is to present the chemical characteristics of this substance and to discuss its relation to various biological functions of vitamin C, mainly as an antioxidant barrier (we analysed product of reaction between phenothiazine derivative and L-ascorbic acid).
This review describe the generation of free radicals in the cells under the influence of exogenously and endogenously acting factors.The interactions of free radicals with proteins and amino acids and the consequences of these effects are also presented.
The role of free radicals as well as cytokines (IL-1, tumor necrosis factor alpha, interferon gamma) and nitric oxide in the immune-mediated processes leading to the beta-cell destruction during IDDM is described.It is also pointed that the excess of IL-1ra in relation to IL-1 prevents IL-1 toxicity to beta-cells.
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This mini review gives a brief overview over the oxidation mechanism of methionine (Met), relevant for processes which may lead to the oxidation of amyloid beta-peptide (betaAP), involved in the pathogenesis of Alzheimer?s disease. The Cu II-catalysed oxidation of C-terminal Met 35 in AP depends on the secondary structure of the peptide. That seems to be the key to the known propensities of this peptide to form reactive oxygen species and free radicals. The pro-oxidant character of betaAP is not associated with its -beta sheet insoluble form. On the contrary, the alpha-helically organised structure is responsible for betaAP redox-related cytotoxicity.
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