Vol. 38 , No. 5, 1995 Printed ill U.S.A.Th e protecti ve effects of high dose antenatal vitam in E on hypoxemi a in newb orn rats were inves tiga ted. The subjects we re l-d-cld Wistar rats we ig hing 5-6 g whi ch were born to mothers weighing 245-250 g. Thr ee groups of rat pups , each consisting of eight newb orn rats, were used: non treated control group, hypoxic gro up, and vitamin E gro up. Th e moth ers of pups in the last gro up were given vitamin E (2000 mg/kg/d) antenatally on 3 consec utive days. Hypoxia was induc ed by breathing of a mixture of 8% oxygen and 92% nitrogen for 3 h. Then pups we re allowed to inhale norm al atmospheric air for 30 min. All rats were killed on the first day of life after the procedure of hypoxia and reoxygenatio n. The brains, lungs, livers, intestin es, and kidneys were studied biochemi cally and histopatholog ically. The hypoxia-indu ced biochemi cal changes were determined by measuring lipid peroxidation and myelopero xidase activity. Vitam in E effectively inhibi ted hypox ia-indu ced lipid peroxid ation in liver and intestines, and dec reased the levels of thiobarbituric Hypoxia and ischemia are major problems in the neonate despit e advanced antenatal and neonat al care. No specific treatment has been shown to improve the high morbidity and mortality associated with this problem .Among many factors that adversely effect the function of placenta in the gas exchange between the fetus and the mother are maternal hypoperfusion induc ed by anesthesia, uterine hypertonicity, abrupti o placenta, and obstruction of the umbilical cord. An y episode of fetal hypoperfusion can cause mild or severe fetal hypoxemia (1). After the reintroduction of oxygen, large amounts of oxygen-free radicals are produced. These radicals can initiate lipid peroxidati on and attack other biologic targets (2-4).Low levels of oxygen radicals produced under physiologic conditions are effectively removed or scave nged by enzymatic and nonen zymati c antioxidant syste ms of the body (5, 6). However, under several pathologic conditions these antioxidant mechanisms may be overw helmed by radicals produ ced in excessive amounts.