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-tocopherols, labeled with different amounts of deuterium [2R,4'R,8'R-alpha-[5-C2H3]tocopheryl acetate (d3RRR-alpha-tocopheryl acetate] and 2RS, 4'RS, 8'RS-alpha-[5,7-(C2H3)2]tocopheryl acetate (d6all rac-alpha-tocopheryl acetate), was studied in adult beagle dogs that had 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 the activity of the hepatic tocopherol binding protein (which is thought to preferentially incorporate RRR-alpha-tocopherol into the plasma) is up-regulated by vitamin E deficiency. Labeled alpha-tocopherols increased and decreased similarly in plasma of both -E and +E dogs. Irrespective of diet, d3RRR-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 also studied vitamin E transport in a German Shepherd dog with degenerative myelopathy (DM). Based on the coincident appearance of d3RRR-alpha-tocopherol in plasma and chylomicrons, we suggest that the abnormality in DM may be associated with abnormal vitamin E transport resulting from an impaired function of the hepatic tocopherol binding protein.