Antioxidative vitamins in prematurely and maturely born infants.
Postnatally a rapid change occurs from a relatively hypoxic to a relatively hyperoxic environment, especially during artificial ventilation with all risks of ROS-formation. Among the non enzymatic antioxidative strategies the vitamins E, C, A and B2 are of major importance. Vitamin E is considered the most important radical scavenging vitamin of the lipid soluble compartment. Hereby vitamin E itself is converted into a radical which is handed over to vitamin C and glutathione into the water soluble compartment. The vitamin E content of the fetus increases with the fetal fat mass mainly during the last trimester of pregnancy. Placenta is only slightly permeable to lipid soluble vitamins. Vitamin E deficiency may rapidly develop typically at about 6-8 weeks of age. Vitamin E is able to prolong significantly the onset of retinopathic changes during oxygen therapy and may prevent intraventricular hemorrhage. Vitamin C is together with glutathione a major representative of the non enzymatic antioxidative system in the water soluble compartment. The best determinant of the vitamin C status is its concentration in leukocytes. Vitamin C reduces iron to the divalent state which supports the hydroxyl radical formation (Haber-Weiss reaction). This should be considered mainly in cases of intraventricular hemorrhage. Vitamin B2 acts mainly as cofactor of glutathione reductase which keeps glutathione in the reduced state. It can therefore be considered an indirect antioxidative vitamin. Vitamin B2 is destroyed by light. Phototherapy has been recognized as a cause of riboflavin deficiency. Vitamin A comprises all retinols with properties like trans-retinol. Retinol storage in the fetal liver increases during late pregnancy. In both, premature and mature newborns, the serum concentrations amount to only about 50% of those of their mothers. Vitamin A has a paramount importance for fetal lung development, because the individual surfactant proteins are selectively regulated by retinoic acid.
Böhles
H
H
Johann-Wolfgang-Goethe-Universität, Frankfurt, Germany.
D000975:Antioxidants; D001205:Ascorbic Acid / Q000502:physiology; D006801:Humans; D007231:Infant, Newborn / Q000502:physiology*; D007234:Infant, Premature / Q000502:physiology*; D012256:Riboflavin / Q000502:physiology; D014801:Vitamin A / Q000502:physiology; D014810:Vitamin E / Q000502:physiology; D014815:Vitamins / Q000502:physiology*
D000975:Antioxidants; D014815:Vitamins; D014801:Vitamin A; D014810:Vitamin E; D001205:Ascorbic Acid; D012256:Riboflavin