Gestation confers temporary resistance to peroxidation in the maternal rat brain.

Lipid peroxidation, as assessed by the formation of thiobarbituric acid substances on incubation with ascorbate-Fe2+, NADPH-ADP-Fe3+ and cumene hydroperoxide in brain homogenate and mitochondria, was significantly decreased during gestation and restored to respective control levels post partum. The decrease observed with the brain homogenate on Day 10 of pregnancy was 42% with ascorbate-Fe2+ and 70% with NADPH-ADP-Fe3+. This temporary decrease in peroxidation potential seems to be due to lesser availability of substrate in the form of unsaturated fatty acids besides increase in the cholesterol:phospholipid ratio and glutathione. Progesterone, the gestational steroid elaborated during pregnancy, inhibited lipid peroxidation in brain mitochondria in a dose-dependent manner. The observed temporary decrease in peroxidation potential may be a special adaptation to protect membranes in the brain against oxidant stress during pregnancy.