Newborn infants are generally thought to be in a vitamin E-deficient state due to their low plasma tocopherol levels and increased hemolysis of red blood cells (RBCs) induced by hydrogen peroxide (HPT). However, the tocopherol in plasma lipids of newborn infants is within an acceptable range because of the low plasma lipids in neonates. In addition, RBC tocopherol levels in the majority of newborn infants, even if they have a very low birth weight, showed a normal vitamin E status immediately after birth, despite the increased susceptibility of their RBCs to HPT. The incresed susceptibility of RBC ghosts in cord blood to oxidant stress was studied using an azo-compound. After vitamin E was exhausted in the ghosts, the oxygen uptake rate was faster in cord ghosts than in adult ghosts, resulting from the fact that the cord ghosts had a higher bisallylic hydrogen content. This finding indicates a relative deficiency of vitamin E in neonatal biomembranes with a sufficient vitamin E content. In addition, vitamin E concentrations in leukocytes, platelets and buccal mucosal cells, othe than those in plasma and RBCs, showed a lower tocopherol level in cord blood cells, as compared with those in older children. The above finding indicates that a higher amount of vitamin E is required by neonates. Wilson's disease and homocystinuria were further investigated. Copper unassociated with ceruloplasmin and a large amount of homocystein both generated superoxide in association with SH groups and ferrous iron, respectively. The generated free radicals induced from superoxide were thought to initiate cell membrane damage in RBC from patients with Wilson's disease, whereas they were found to produce modified LDL in the reaction of homocystein with ferric iron. These changes seem to be related to the development of hemolytic crisis in Wilson's disease and the early onset of atherosclerosis in patients with homocystinuria. Oxidation of LDL resulting from homocysteine and ferric iron will be prevented by a high concentration of tocopherol in LDL, while oxidative stress due to non-ceruloplasmin Cu will be inhibited by zinc ion.
