Abstract
Products of per oxide lipid oxidation are produced in the place of increased oxidative stress and their accumulation leads to aterotic damage. Most of the investigations are still devoted to formation and oxidized lipid metabolism, but the data on their biological activity and possible pathophysiological functions are not many. In this review it was done an attempt to analyze the mechanisms of formation, metabolic activity and by transforming the cholesterol ester, which contain the unsaturated fatty acids, that may oxidize to form peroxides. The last are able to be restored to appropriate alcohols, which can be oxidized to biologically active aldehydes, which make a significant contribution to the development of progressive atherosclerotic lesions.The most cholesterol esters are as a part of ß – lipoproteins, localized in the hydrophobic core and in doing so are able to be oxidized hydro peroxides faster than the outer layer of phospholipids. Most of aldehydes, which are formed at per ester oxidation – these are nine–, eight– and five carbon compounds. Because of cholesterol esters in ß – lipoprotein were formed mainly by linoleic acid, therefore its level was reliable test of per oxidation degree of these esters.The analysis of stereoisomers of oxidized lipids, which were marked from atherogenic plaques, witnessed a significant contribution of the enzyme lipooxi genesis in oxidative modification of cholesterol esters. Selenium containing enzymes play an important role in the metabolism of cholesterol hydroxides esters, in particular: glutathionereductase and tioredoxinereductase. It was also obtained the convincing data on the participation of aldosereductase in these processes.Esther of cholesterol inhibit the mitotic activity of growth factor of atherogenic plaques, fibroblast growth factor and the ß1– antiproliferative activity of transforming growth factor.Hence, oxidative modification of lipids in general, oxidized of cholesterol esters and in particular, is one of the causes of progressive development of atherosclerotic damages, Although metabolic pathway of lipoprotein particles to the atherosclerotic plaque is search enough.
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