Are lipid peroxidation processes induced by changes in the cell wall structure and how are these processes connected with diseases?
Apparently nature uses the unique sensitivity of polyunsaturated fatty acids (PUFAs) versus oxygen to generate chemical signals if the surface of a cell is influenced by an outside or inside event; for instance the attack of microorganisms, proliferation, aging or by treatment of isolated cells with surfactants. It seems that mammalian and plant cells respond equally to such changes in their structures by transformation of polyunsaturated fatty acids localized in the phospholipid layer of the cell wall to lipidhydroperoxides (LOOHs). These lipid peroxidation (LPO) processes involve all PUFAs, not only arachidonic acid.Slight physiological changes of the cell wall for instance by proliferation seem to activate enzymes, e.g., phospholipases and lipoxygenases (LOX). When an outside impact (for instance by attack of microorganisms) exceeds a certain level LOX commit suicide and liberate iron ions. These start a nonenzymatic LPO. Enzymatic and nonenzymatic LPO distinguish fundamentally which has not been recognized in the past. In the enzymatic LPO processes peroxyl radicals generated as intermediates cannot leave the enzyme complex. In contrast in a nonenzymatic LPO process peroxyl radicals are not trapped. They attack nearly any kind of biological molecules, for instance proteins. Thus only the amount of an outside impact decides if proliferation, apoptosis, or necrosis is started. Some evidence indicates that cancer might be the consequence of a low response of cells to induce apoptotic LPO processes. In contrast to high level of LPO processes induces diseases combined with inflammation, for instance rheumatic arthritis. After consumption of food rich in linoleic acid its LPO products become increased in low density lipoprotein (LDL). This LDL is able to enter endothelial cells and damage cells from inside, long before an inflammatory response is detectable.
Spiteller
Gerhard
G
Lehrstuhl Organische Chemie, Universitätsstrasse 30, Bayreuth, Germany. gerhard.spiteller@uni-bayreuth.de
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001161:Arteriosclerosis / Q000209:etiology / Q000378:metabolism; D002455:Cell Division / Q000502:physiology; D002473:Cell Wall / Q000378:metabolism*; D005231:Fatty Acids, Unsaturated / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology*; D008563:Membrane Lipids / Q000378:metabolism; D008954:Models, Biological; D009369:Neoplasms / Q000209:etiology / Q000378:metabolism; D019636:Neurodegenerative Diseases / Q000209:etiology / Q000378:metabolism; D010545:Peroxides / Q000378:metabolism; D015398:Signal Transduction
D005231:Fatty Acids, Unsaturated; D008563:Membrane Lipids; D010545:Peroxides; C049375:perhydroxyl radical