Ovarian vitamin E accumulation: evidence for a role of lipoproteins.

Reactive oxygen species, such as superoxide, hydrogen peroxide, and lipid peroxides, impair luteal function. Vitamin E, a lipophilic antioxidant vitamin, provides a major avenue of protection by scavenging free radicals and terminating lipid peroxidation. We previously showed that ovarian vitamin E levels increase after functional regression (loss of progesterone production) of the corpus luteum in the pseudopregnant rat and the objective of the present studies was to determine the mechanism(s) that resulted in such increased levels of vitamin E. Luteal vitamin E levels were significantly elevated after function regression and remained elevated. Luteal cholesterol ester levels, in contrast, decreased in parallel with the decrease in plasma progesterone levels, whereas plasma vitamin E, cholesterol, and cholesterol ester levels did not change. Because vitamin E is transported in blood by chylomicrons and lipoproteins, ovarian vitamin E levels were determined after treatments known to modify ovarian lipoprotein receptor content and serum lipoproteins. Acute treatment with aminoglutethimide during the mid-luteal phase decreased serum progesterone levels and increased luteal vitamin E and cholesterol ester levels. Daily treatment with 4-amino-pyrazolo-(3,4-d)pyrimidine reduced serum vitamin E and cholesterol ester levels, diminished the accumulation of vitamin E associated with luteal regression, significantly reduced luteal cholesterol esters levels, and increased luteal high density lipoprotein-binding sites. Analysis of the distribution of vitamin E between a membrane/particulate pellet and a lipid droplet/granule cytosol before and after luteal regression revealed no changes. Vitamin E levels were divided 60:40 between a crude particulate/membrane fraction and a cytosol/lipid droplet fraction, although functional regression produced a 2.5-fold increase in total luteal vitamin E levels. In conclusion, the uptake of vitamin E by the corpus luteum appears to be mediated by lipoprotein receptors and the increase in vitamin E that follows functional regression, we suggest, may be due to a diminished consumption of vitamin E by oxidative radicals, most likely generated during steroidogenesis.