[Cell damage as reason for the formation of unsaturated fatty acid hydroperoxides]

Abstract

In diseases leading to massive acute cell damage, e.g., myocardial infarction or spontaneous inflammation, increased amounts of hydroperoxides of unsaturated fatty acids (LOOH) are found. An even higher production of LOOH is observed in homogenized tissue. If cells are injured, dormant lipoxygenases (LOX) are inevitably activated. They oxidize unsaturated membrane fatty acids to LOOH. This process involves not only arachidonic acid - as tacitly assumed up to now - but also linoleic acid. LOOH are decomposed to chemically highly reactive species, some of which were previously unknown (e.g, alpha-hydroxyaldehydes). LOO. radicals can also transform any molecule with a double bond to an epoxide. Therefore, epoxides are found in injured tissue. The same degradation products of hydroperoxides have been observed in elevated amounts in acute cell injury and in chronic diseases, e.g., atherosclerosis, psoriasis, and rheumatoid diseases. Therefore, we conclude that in these cases too, increased generation of hydroperoxides is caused by gradual cell injury liberating lipoxygenases.