Abstract
The influence of oxidative stress in rat brain and liver on intrauterine growth retardation (IUGR) in rat fetuses was examined. Twenty pregnant Wistar rats were used. On the 15th day of pregnancy, uterine artery and vein were ligated bilaterally using a modified Wigglesworth method. On the 21st day of pregnancy, the fetuses were delivered by hysterotomy. Fetal blood was collected by cardiac puncture. Fetal brain and liver were removed for the analysis of lipid peroxide. Sham surgical operations were performed in the control rats. Within the ligated group, a superoxide dismutase mimicking substance, Fe-chlorine e6-Na (FeCNa), was injected intraperitoneally once a day from day 15 of gestation to day 20. Fetal blood, brain, and liver were stored at –70°C until analysis. Control rats received an equivalent volume of saline. In growth-retarded fetuses, both superoxide released from erythrocytes and brain lipid peroxide showed significantly higher levels, but not superoxide dismutase in erythrocytes and liver lipid peroxide. These changes were alleviated by injection of superoxide dismutase-mimicking substance, FeCNa. Rat fetuses with intrauterine growth retardation suffered from a significant oxidative stress in utero. The increase in reactive oxygen species was alleviated by an injection of FeCNa.
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