OVARIAN VITAMIN-E ACCUMULATION - EVIDENCE FOR A ROLE OF LIPOPROTEINS

Reactive oxygen species, such as superoxide, hydrogen peroxide, and li pid peroxides, impair luteal function. Vitamin E, a lipophilic antioxi dant vitamin, provides a major avenue of protection by scavenging free radicals and terminating lipid peroxidation. We previously showed tha t 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 mec hanism(s) that resulted in such increased levels of vitamin E. Luteal vitamin E levels were significantly elevated after functional regressi on and remained elevated. Luteal cholesterol ester levels, in contrast , decreased in parallel with the decrease in plasma progesterone level s, whereas plasma vitamin E, cholesterol, and cholesterol ester levels did not change. Because vitamin E is transported in blood by chylomic rons and lipoproteins, ovarian vitamin E levels were determined after treatments known to modify ovarian lipoprotein receptor content and se rum lipoproteins. Acute treatment with aminoglutethimide during the mi dluteal 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 est er levels, diminished the accumulation of vitamin E associated with lu teal regression, significantly reduced luteal cholesterol esters level s, and increased luteal high density lipoprotein-binding sites. Analys is of the distribution of vitamin E between a membrane/particulate pel let and a lipid droplet/granule cytosol before and after luteal regres sion revealed no changes. Vitamin E levels were divided 60:40 between a crude particulate/membrane fraction and a cytosol/lipid droplet frac tion, although functional regression produced a 2.5-fold increase in t otal luteal vitamin E levels. In conclusion, the uptake of vitamin E b y the corpus luteum appears to be mediated by lipoprotein receptors an d the increase in vitamin E that follows functional regression, we sug gest, may be due to a diminished consumption of vitamin E by oxidative radicals, most likely generated during steroidogenesis.