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The effect of high dose antenatal vitamin E on hypoxia-induced changes in newborn rats
Insights
High-dose antenatal vitamin E supplementation protected newborn rats against tissue damage from hypoxia. This vitamin E treatment reduced lipid peroxidation and inflammatory markers, suggesting a protective role in neonatal hypoxemia.
Area of Science:
- Neonatal physiology
- Biochemistry
- Histopathology
Background:
- Neonatal hypoxemia can cause significant tissue injury.
- Vitamin E is an antioxidant with potential protective properties.
Purpose of the Study:
- To investigate the protective effects of high-dose antenatal vitamin E against hypoxia-induced tissue injury in newborn rats.
Main Methods:
- Wistar rat pups were exposed to hypoxia (8% oxygen) for 3 hours.
- Mothers received high-dose vitamin E antenatally.
- Biochemical (lipid peroxidation, myeloperoxidase activity) and histopathological analyses were performed on various organs.
Main Results:
- Vitamin E inhibited hypoxia-induced lipid peroxidation in the liver and intestines.
- It decreased thiobarbituric acid-reactive substances in the brain.
- Vitamin E prevented increased myeloperoxidase activity and histopathological damage in the intestines and liver.
Conclusions:
- High-dose antenatal vitamin E demonstrates protective effects against hypoxia-induced tissue injury in newborn rats.
- Vitamin E may mitigate oxidative stress and inflammation associated with neonatal hypoxemia.
Abstract:
The protective effects of high dose antenatal vitamin E on hypoxemia in newborn rats were investigated. The subjects were 1-d-old Wistar rats weighing 5-6 g which were born to mothers weighing 245-250 g. Three groups of rat pups, each consisting of eight newborn rats, were used: nontreated control group, hypoxic group, and vitamin E group. The mothers of pups in the last group were given vitamin E (2000 mg/kg/d) antenatally on 3 consecutive days. Hypoxia was induced by breathing of a mixture of 8% oxygen and 92% nitrogen for 3 h. Then pups were allowed to inhale normal atmospheric air for 30 min. All rats were killed on the first day of life after the procedure of hypoxia and reoxygenation. The brains, lungs, livers, intestines, and kidneys were studied biochemically and histopathologically. The hypoxia-induced biochemical changes were determined by measuring lipid peroxidation and myeloperoxidase activity. Vitamin E effectively inhibited hypoxia-induced lipid peroxidation in liver and intestines, and decreased the levels of thiobarbituric acid-reactive substances in brain. In agreement with lipid peroxidation, tissue associated myeloperoxidase activity was increased in liver, intestines, and kidneys, but not in brain and lungs, of the hypoxic group. Histopathologic changes in intestines were epithelial separation and submucosal polymorphonuclear leukocyte infiltration. In the liver, leukocyte infiltration was observed only near the portal areas. These changes were not observed in the vitamin E group. It was concluded that high doses of antenatal vitamin E may protect the newborn rat pups against hypoxia-induced tissue injury.