Enzymic lipid peroxidation-α consequence of cell injury?

It is postulated that cell injury activates “dormant” enzymes to produce lipid hydroperoxides. In a first step, membrane lipids are cleaved by esterases. The unsaturated fatty acids thus produced are converted in a second step by lipoxygenases to lipid hydroperoxides (LOOHs). In a third, nonenzymic step, these LOOHs, together with dienoic hydroxy fatty acids produced by enzymic reduction of LOOHs, react with a second oxygen molecule to generate dihydroperoxy-fatty acids and hydroxy-hydroperoxy-fatty acids, which are degraded to a-hydroxyaldehydic compounds. This last reaction requires production of LOʹ-radicals by iron ions that also are generated as a result of cell damage. In addition, α-hydroxyaldehydes are produced by hydrolysis of plasmalogen epoxides, which are generated by oxidation of plasmalogens with LOOʹ or by action of epoxidases. We hypothize that α-hydroxyaldehydes act as second messengers. The release of lipoxygenase and the consequent lipid hydroperoxidation is postulated to occur in massive cell damage (e.g., myocardial infarction), in chronic diseases such as rheumatism, diabetes and atherosclerosis, in aging, and in control of cell proliferation.