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Trans-arachidonic acids: new mediators of inflammation Balazy MJ Physiol Pharmacol 2000[Dec]; 51 (4 Pt 1): 597-607Inflammation and many other pathological processes lead to increased production of free radicals that target critical macromolecules such as proteins, DNA and lipids. Structural modifications of these molecules, induced by free radicals, typically result in alterations of vital biochemical processes. Hydroxyl radical-initiated lipid peroxidation is known to generate a variety of toxic oxidized lipids, many of which originate from polyunsaturated fatty acids esterified to cellular membrane phospholipids. Recent interests have focused on a group of lipids known as isoeicosanoids that are formed from peroxidation of arachidonic acid, and share structural similarity to enzymatically-derived prostaglandins and leukotrienes. However, little is known about lipid peroxidation processes initiated by nitrogen free radicals. NO2 is a toxic free radical and an abundant urban air pollutant, which is also generated in vivo from oxidations of nitric or nitrite and decomposition of peroxynitrite. The NO2-induced lipid peroxidation mechanisms involving arachidonic acid have not been characterized. Described here is the isomerization of arachidonic acid, a new process induced by NO2, which leads to a mixture of trans-arachidonic acids. We observed that the levels of trans-arachidonic acids in rat plasma increased following infusion of bacterial endotoxin; therefore, the isomerization of arachidonic acid is likely to occur in vivo by a mechanism involving NO2.|Animals[MESH]|Arachidonic Acid/chemistry/*metabolism[MESH]|Free Radicals/*metabolism[MESH]|Humans[MESH]|Inflammation Mediators/*metabolism[MESH]|Lipid Peroxidation[MESH]|Nitrogen Dioxide/chemistry/*metabolism[MESH]|Stereoisomerism[MESH]|Systemic Inflammatory Response Syndrome/physiopathology[MESH] |
