Some recent studies have reported that low-density lipoprotein (LDL) isolated from estrogen-treated postmenopausal women exhibited increased oxidation resistance ex vivo. However, the underlying mechanisms responsible for this effect are not clear. We explored the possibility that lipophilic derivatives of 17β-estradiol (E 2 ) could be incorporated into LDL and high-density lipoprotein (HDL) particles inhibiting lipoprotein oxidation. Introduction of small amounts of esterified E 2 into lipoproteins by means of incubation of free E 2 and E 2 17-stearate in plasma did not result in any antioxidant effect. Using an artificial transfer system (Celite dispersion), larger amounts of E 2 esters could be incorporated into lipoproteins. Concentrations ranging between 0.27 and 1.38 molecules/LDL particle for E 2 17-stearate and between 0.36 and 1.93 molecules/LDL particle for E 2 17-oleate resulted in increased Cu 2 + -induced oxidation resistance of LDL as indicated by statistically significant lag time prolongations. Significant prolongations of lag times were also observed for HDL following incorporation of E 2 esters using Celite as transfer system. Our results suggest that free E 2 can be esterified and incorporated into lipoproteins during incubation in plasma. However, incorporation of supraphysiologic concentrations of E 2 esters into lipoproteins by means of the artificial transfer system was required in order to reduce their oxidation susceptibility.