Increased rate of lipid peroxidation and protein carbonylation in experimental diabetic pregnancy

Aims/hypothesis. Maternal Type I (insulin-dependent) diabetes mellitus is associated with an increased risk for fetal malformations and spontaneous abortions. Although the pathogenic mechanism is not fully understood, reactive oxygen species have been shown to contribute to the pathogenesis in experimental studies. By measuring 8-iso-PGF(2 alpha) and protein carbonyls, radical oxygen damage to lipids and proteins can be estimated. The aim of this study was to investigate the status of lipid peroxidation and protein carbonylation in mothers and fetuses in experimental diabetic pregnancy. Methods. Non-pregnant and pregnant rats with and without streptozotocin-induced diabetes were studied after 4 weeks of diabetes or at gestational day 19, respectively Gross morphology of the offspring was studied and 24 h urine, plasma, amniotic fluid, maternal and fetal Livers were collected. Concentrations of 8-iso-PGF(2 alpha), 15-keto-DH-PGF(2 alpha) and other oxidative stress variables were measured. Results. Malformation and resorption rates were increased in diabetic litters, whereas fetal weights were decreased in the control rats. There were no statistically significant differences in maternal plasma concentrations of 8-iso-PGF(2 alpha), but plasma protein carbonyl content was increased in the diabetic groups. Pregnancy increased 24 h urinary excretion of 8-iso-PGF(2 alpha) in diabetic rats but not in the control rats. There was no difference in the amniotic fluid concentration of 8-iso-PGF(2 alpha) between the normal and the diabetic group. However, in the diabetic group there was a correlation between the uterine horn concentration of 8-iso-PGF(2 alpha) and the percentage of resorptions. Conclusions/interpretation. In diabetic pregnancy, both diabetes and pregnancy are promoting oxygen radical damage. Fetal oxidative stress markers do not clearly reflect fetal morphology.