Atherosclerosis is a chronic pathological process in which inflammatory factors play an important role. Eicosanoid-lipid derivatives of three polyunsaturated 20-carbon fatty acids play the key role in the course of inflammatory reactions. The most common of them is arachidonic acid which is the main precursor of eicosanoids in macrophages. Eicosanoids are unstable, locally acting tissue hormones some of which are responsible for stimulation of the atherosclerotic process, e.g. by regulating expression of genes involved in growth, apoptosis and migration of cells within the atherosclerotic plaque.

CLAs are fatty acids which may be used in prophylaxis of civilisation diseases (including atherosclerotic disease). Potential anti-atherosclerotic functions of CLAs were demonstrated in animal studies. The observations on animals allowed hopes that CLAs might found an application in the prophylaxis of atherosclerosis in humans. However, intensification of oxidation reactions (by the diet supplementing trans-10, cis-12 CLA isomer) observed in humans indicated the existence of risks associated with the use of these acids as dietary supplements. The present study, which examines the effect of CLAs on arachidonic acid metabolism in macrophages, is an attempt to find an answer to the question whether CLAs may be used in the prophylaxis of atherosclerosis in humans. The investigations focused on macrophages - the cells which play the central role in the atherosclerotic process. In vitro investigations aimed to improve the understanding of the mechanisms of conjugated linoleic acid (CLA) dienes effects on arachidonic acid and linoleic acid metabolism in macrophages from a cell line and from peripheral blood.

Basing on the results, the following conclusions have been drawn:

1. CLAs may be incorporated into macrophage membrane phospholipids, reducing content of arachidonic acid.
2. CLAs may reduce the activity of phospholipases in macrophages, through which they may reduce arachidonic acid availability for other enzymes such as 15-lipoxygenase and cyclooxygenases.
3. cis-9, trans-11 CLA may inhibit the intensity of phosphorylation of cellular MAP p42/p44 (ERK-1/ERK-2) kinases, thus contributing to reduced activity of phospholipases A₂.
4. CLAs enhance the synthesis of reactive oxygen species (ROS) in the cell.
5. Increased ROS production with concomitant inhibition of PLA₂ activity may lead to an increase in free-radical oxidation of ARA to isoprostanes.
6. CLAs contribute to increased CD36 expression in vitro.
7. CLAs are a factor limiting the activation of NF-κB, thus contributing to an inhibition of COX-2 expression.
8. CLAs may be a direct regulator of enzymatic activity, e.g. the activity of COX-1; they may also be regulators of enzyme expression, eg. sPLA₂ or COX-2.

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