Inflammation plays a relevant role in the onset and development of atherosclerosis and cardiovascular disease; its nutritional or pharmacological control is the aim of several studies [1]. At the crossroad between nutrition and pharmacology, long-chain n ? 3 (or omega 3) fatty acids, namely docosahexaenoic
IU1 inhibitor (DHA, 22:6n ? 3) and eicosapentaenoic acid (EPA, 20:5n ? 3) have been attributed cardioprotective properties [2]. While the mechanisms underlying these effects are manifold, their anti-inflammatory activities are being actively explored. Part of the anti-inflammatory properties of n ? 3 fatty acids might be due to their replacing n ? 6 fatty acids, namely arachidonic acid (ARA, 20:4n ? 6), in phospholipids, thus providing different substrates for pro-inflammatory secreted phospholipases A2 (sPLA2) [3]. Also, direct activities of n ? 3 fatty acids on inflammation-related enzymes such as cycloxygenase-2 (COX-2) have been demonstrated [4] and there is accumulating evidence of their antioxidant properties, both direct and indirect [5]. Among the cellular sources of oxidants, NADPH oxidases (Noxs) catalyze electron transfer from NADPH onto molecular O2 [6]. This process generates reactive oxygen species (ROS), namely superoxide anion (O2?) and, when deregulated, contributes to the development of endothelial dysfunction, smooth muscle cell growth, and inflammation [7]. Of the several NADPH oxidase isoforms, Nox 4 is highly expressed in endothelial
cells [7] and is a major contributor to ROS generation.