Docosahexaenoic acid trials in cystic fibrosis: A review of the rationale behind the clinical trials  S. Van Biervliet, J.P. Van Biervliet, E. Robberecht, A. Christophe  Journal of Cystic Fibrosis  Volume 4, Issue 1, Pages 27-34 (March 2005) DOI: 10.1016/j.jcf.2004.11.001 Copyright © 2004 European Cystic Fibrosis Society Terms and Conditions

Fig. 1 Fatty acid notation: number of carbon atoms: number of double bonds followed by biochemical series. Journal of Cystic Fibrosis 2005 4, 27-34DOI: (10.1016/j.jcf.2004.11.001) Copyright © 2004 European Cystic Fibrosis Society Terms and Conditions

Fig. 2 Arachidonic acid is released by the action of phospholipase A2 on membrane phospholipids. Phospholipase A2 is activated by multiple cell signals, bradykinin, angiotensin II. Some derivatives of alpha-linolenic acid, the essential fatty acid of the ω-3 series, inhibit the release of arachidonate by phospholipase A2, and result in antagonistic actions. The three main directions of the metabolism of arachidonate are cyclooxygenation, lipoxygenation and epoxygenation. The cyclooxygenase products of arachidonate generate prostaglandins, prostacyclin and thromboxanes of the 2 series. Lipoxygenase products of arachidonate generate the pro-inflammatory leukotrienes, but also some biologically very active hydroperoxyeicosatetranoates (HETEs) and the anti-inflammatory lipoxins. The epoxgenation pathways result, by action of cytochromes P450, in formation of 3 categories of biologically very active products: midchain HETEs, ω-terminal HETEs and epoxyeicosatrienoic acids (EETs). Journal of Cystic Fibrosis 2005 4, 27-34DOI: (10.1016/j.jcf.2004.11.001) Copyright © 2004 European Cystic Fibrosis Society Terms and Conditions