Abstract

Objective: The atherogenicity of low-density lipoproteins (LDLs) is greatly enhanced when LDL is modified, particularly by oxidation. Experimental data as well as studies in rabbits and monkeys suggest an anti-oxidant effect of estrogens that results in reduced formation of oxidized LDL. Oxidized LDL in plasma is rapidly cleared from the circulation by means of scavenger receptors, and it is difficult to demonstrate direct changes using plasma samples only. The oxidative potential for the formation of oxidized LDL is derived from the polyunsaturated fatty acids of the phospholipid lecithin. For example, an increase in the relative content of linoleic and arachidonic acids in serum lecithin could tentatively be regarded as a decrease in the formation of oxidized LDL. Design: Forty perimenopausal women were given continuous hormone replacement therapy (HRT) consisting of 2 mg of estradiol daily. After random allocation, levonorgestrel comedication was given as 0.250-mg tablets for 10 days per cycle or was continuously released (0.02 mg/d) from an intrauterine device (IUD). The relative fatty acid composition of serum lecithin was determined by gas-liquid chromatography using a capillary column equipped with a flame ionization detector and a computerized identification system based on retention times. Results: Polyunsaturated acids in serum lecithin were augmented by both regimes with negligible differences between the oral and the IUD group. Conclusions: The present results indicate that estradiol in combination with either oral cyclical or continuous-release levonorgestrel inhibits formation of oxidized LDL.

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