Effect of estradiol ethynyl and estradiol propionate on esterification of saturated and non-saturated fatty acids in liver tissue, as one of possible mechanisms in development of estrogen-induced hypertriglyceridemia, was studied using labelled precursors 3H-palmitic and 14C-linoleic acids. Both these estrogens stimulated the incorporation of exogenous fatty acids into triglycerides. After administration of estradiol dipropionate relative esterification of 14C-linoleic acid into triglycerides was increased as compared with controls. Estradiol ethynyl increased and estradiol dipropionate decreased the incorporation of exogenous fatty acids into liver phospholipids. Both estrogens activated the relative esterification of linoleic acid into phospholipids. A decrease in exogenous fatty acids esterification into fraction of cholesterol esters, caused by both these estrogens, occurred due to an increase in relative incorporation of linoleic acid into these lipids. As shown in experiments of relative esterification of saturated and non-saturated fatty acids, estradiol propionate stimulated synthesis of more non-saturated forms of triglycerides, phospholipids and cholesterol esters in rat liver tissue as compared with the estradiol ethynyl action. The data obtained and the data of literature suggest that activation of exogenous fatty acids esterification into triglycerides and alterations in relative esterification of saturated and non-saturated fatty acids into triglycerides and phospholipids of liver tissue are of importance in pathogenesis of estrogen-induced hypertriglyceridemia.