Increased rate of lipid peroxidation and protein carbonylation in experimental diabetic pregnancy.
OBJECTIVE
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-PGF2alpha 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-PGF2alpha, 15-keto-DH-PGF2alpha 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-PGF2alpha, but plasma protein carbonyl content was increased in the diabetic groups. Pregnancy increased 24 h urinary excretion of 8-iso-PGF2alpha in diabetic rats but not in the control rats. There was no difference in the amniotic fluid concentration of 8-iso-PGF2alpha between the normal and the diabetic group. However, in the diabetic group there was a correlation between the uterine horn concentration of 8-iso-PGF2alpha and the percentage of resorptions.


CONCLUSIONS
In diabetic pregnancy, both diabetes and pregnancy are promoting oxygen radical damage. Fetal oxidative stress markers do not clearly reflect fetal morphology.
Cederberg
J
J
Department of Medical Cell Biology, Uppsala University, Sweden.
Basu
S
S
Eriksson
U J
UJ
D000653:Amniotic Fluid / Q000378:metabolism; D000818:Animals; D000013:Congenital Abnormalities / Q000209:etiology; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000150:complications / Q000378:metabolism / Q000652:urine; D015237:Dinoprost / Q000031:analogs & derivatives* / Q000378:metabolism; D028441:F2-Isoprostanes / Q000378:metabolism; D005260:Female; D005327:Fetal Resorption / Q000209:etiology; D008054:Lipid Peroxides / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D011247:Pregnancy; D011256:Pregnancy Outcome; D011254:Pregnancy in Diabetics / Q000097:blood / Q000150:complications / Q000378:metabolism* / Q000652:urine; D011506:Proteins / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012016:Reference Values; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D028441:F2-Isoprostanes; D008054:Lipid Peroxides; D011506:Proteins; D017392:Thiobarbituric Acid Reactive Substances; C008228:15-keto-13,14-dihydroprostaglandin F2alpha; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost