Animal lipoxygenases (EC 1.13.11.12, LOX) convert arachidonic acid to biological active compounds known as eicosanoids. Proinflammatory eicosanoids - leukotrienes are involved in progression of atherosclerosis. Our attention was focused on a connection between activity of LOX and primary hypertriacylglycerolaemia, untreated or treated with fenofibrate. Our results show that LOX activity in the cytoplasm derived from liver of hypertriacylglycerolaemic rats is significantly increased (pH 7,2; relative to the control group), which may be one reason for more rapid atherosclerosis progression in lipid metabolism disorders. The highest LOX activity in microsomes was showed in groups of rats treated with fenofibrate. It appears that fibrates indirectly promote association of LOXs to membranes. In fat fraction no significant effect of hypertriacylglycerolaemia on the activity of lipoxygenase was found. Using gel electrophoresis significantly different spectrum of proteins was discovered in the control samples and samples of hypertriacylglycerolaemic rats. It appears that in condition of lipid metabolism imbalance formation of proteins with low molecular weight (and possibly also expression of LOX) is elevated.