VITAMIN-E-DEFICIENCY IN DOGS DOES NOT ALTER PREFERENTIAL INCORPORATION OF RRR-ALPHA-TOCOPHEROL COMPARED WITH ALL RAC-ALPHA-TOCOPHEROL INTO PLASMA

The plasma and lipoprotein transport of RRR and all rac-alpha- tocophe rols, labeled with different amounts of deuterium [2R,4'R,8'R-alpha-[5 -(CH3)-H-2]tocopheryl acetate (d(3)RRR-alpha-tocopheryl acetate] and 2 RS, 4'RS, 8'RS-alpha-[5,7-((CH3)-H-2)(2)] tocopheryl acetate (d(6)all rac-alpha-tocopheryl acetate), was studied in adult beagle dogs that h ad been fed a vitamin E-deficient (-E; two dogs) or supplemented (+E; two dogs) diet for two years. We set out to test the hypothesis that t he activity of the hepatic tocopherol binding protein (which is though t to preferentially incorporate RRR-alpha-tocopherol into the plasma) is up regulated by vitamin E defiency. Labeled alpha-tocopherols incre ased and decreased similarly in plasma of both -E and +E dogs. Irrespe ctive of diet, d(3)RRR-alpha-tocopherol was preferentially secreted in plasma. Thus, vitamin E deficiency in dogs does not markedly increase the apparent function of the hepatic tocopherol binding protein. We a lso studied vitamin E transport in a German Shepherd dog with degenera tive myelopathy (DM). Based on the coincident appearance of d(3)RRR-al pha-tocopherol in plasma and chylomicrons, we suggest that the abnorma lity in DM may be associated with abnormal vitamin E transport resulti ng from an impaired function of the hepatic tocopherol binding protein .