Lipid peroxidation in developing fetal guinea pig brain during normoxia and hypoxia.

Lipid peroxidation in the fetal guinea pig brain was studied at 30, 35, 40, 45, 50, and 60 days of gestation. Conjugated dienes and fluorescent compounds, indices of lipid peroxidation, peaked at 35 days of gestation, decreased by 45 days, and remained at that level until birth. The higher levels of peroxidation products in early gestational periods (30-40 days) suggest that either the anti-oxidant mechanisms for scavenging oxygen free-radicals and further metabolizing oxidation products are underdeveloped, or the rate of peroxidation is higher than periods near term. Prenatal hypoxia increased the levels of conjugated dienes and fluorescent products in the brains of preterm (50 days) and term (60 days) fetuses. Brain homogenates incubated in air at 37 degrees C underwent rapid lipid peroxidation as measured by the level of thiobarbituric acid (TBA)-reactive substances. However, term brain showed a higher rate of peroxidation and attained higher steady state levels of TBA-reactive substances than preterm brain. This may be due to the higher levels and degrees of unsaturation in fatty acids in term brain. Following hypoxia, term brain showed 5 times the rate of lipid peroxidation and a 3-fold increase in total TBA-reactive substances over controls. These studies show that a significant degree of lipid peroxidation is occurring in the fetal brain during gestation and that the developing brain is more susceptible to lipid peroxidation near term. Furthermore, prenatal hypoxic stress further increases the susceptibility of the brain to peroxidative reactions.