VITAMIN-E - METABOLISM AND ROLE IN ATHERO SCLEROSIS

Vitamin E is the term used for eight naturally occurring fat-soluble n utrients. Alpha-tocopherol predominates in many species and has the hi ghest biological activity. Vitamin E is absorbed via the lymphatic pat hway and transported in association with CM. Vitamin E is carried in p lasma by lipoproteins. II is secreted by the liver in nascent VLDL wit h a preferential incorporation of alpha-tocopherol. Most of the plasma vitamin E is in LDL and in HDL. Vitamin E is exchanged readily betwee n lipoproteins: tocopherol in HDL readily transfers to apolipoprotein B-containing lipoproteins (VLDL, LDL), with little return of tocophero l from the apolipoprotein B-containing lipoproteins to HDL. The mechan isms of tissue uptake of vitamin E from the lipoproteins is poorly und erstood. This uptake may occur during catabolism of triacylglycerol-ri ch lipoproteins by the activity of lipoprotein lipase, via the LDL rec eptor or by nonreceptor-mediated uptake. Vitamin E may act to prevent the initiation/progression of spontaneous atherosclerosis. This concep t is based on in-vitro data: vitamin E influences the responses of cel ls (vascular endothelial cells, leukocytes, vascular smooth muscle cel ls) and the modification of lipoproteins (especially LDL) which, at le ast in principle, could contribute to the initiation/progression of sp ontaneous atherosclerosis. In vivo studies are clearly required to est ablish the extent and mode of vitamin E's antiatherosclerotic impact a nd, hence, its therapeutic potential.