A defect in the activities of Δ6 and Δ5 desaturases and pro-resolution bioactive lipids in the pathobiology of non-alcoholic fatty liver disease

Figure 4 Structures of Resolvin D1 and D2. DHA is converted to 17R-resolvins by a similar aspirin-triggered mechanism similar to the scheme shown in Figure 2. In the absence of aspirin, COX-2 of endothelial cells converts DHA to 13S-hydroxy-DHA. In the presence of aspirin, the initial product is 17R-hydroxy-DHA, which is converted to 7S-hydroperoxy, 17R-hydroxy-DHA by the action of a lipoxygenase, and thence via an epoxy intermediate to epimeric resolvins D1 and D2. An alternative lipoxygenase-generated intermediate, 4S-hydroperoxy, 17R-hydroxy-DHA, is transformed via an epoxide to epimeric resolvins D3 and D4. 17S Resolvins of the D series are produced in cells in the absence of aspirin by a reaction catalyzed in the first step by a lipoxygenase. COX: Cyclo-oxygenase; DHA: Docosahexaenoic acid.