ascorbic-acid and Fetal-Resorption

The aim was to investigate whether dietary supplementation of a combination of the two antioxidants, vitamin E and vitamin C, would protect the fetus in diabetic rat pregnancy at a lower dose than previously used. Normal and streptozotocin-induced diabetic rats were mated and given standard food or food supplemented with either 0.5% vitamin E + 1% vitamin C or 2% vitamin E + 4% vitamin C. At gestational d 20, gross morphology and weights of fetuses were evaluated. Vitamins E and C and thiobarbituric acid reactive substances were measured in maternal and fetal compartments. In addition, protein carbonylation was estimated in fetal liver. Maternal diabetes increased the rate of malformation and resorption in the offspring. High-dose antioxidant supplementation decreased fetal dysmorphogenesis to near normal levels. The low-dose group showed malformations and resorptions at an intermediate rate between the untreated and the high-dose groups. Thiobarbituric acid reactive substances were increased in fetal livers of diabetic rats and reduced to normal levels already by low-dose antioxidative treatment. Protein carbonylation rate was also increased in fetal liver of diabetic rats; it was normalized by high-dose treatment but only partially reduced by low-dose antioxidants. We conclude that combined antioxidative treatment with vitamins E and C decreases fetal malformation rate and diminishes oxygen radical-related tissue damage. However, no synergistic effect between the two antioxidants was noted, a result that may influence future attempts to design antiteratogenic treatments in diabetic pregnancy. Oxidatively modified proteins may be teratogenically important mediators in diabetic embryopathy.

Topics: Animals; Ascorbic Acid; Congenital Abnormalities; Diabetes Mellitus, Experimental; Drug Interactions; Female; Fetal Resorption; Fetus; Liver; Oxidative Stress; Pregnancy; Pregnancy in Diabetics; Pregnancy Outcome; Proteins; Rats; Rats, Sprague-Dawley; Vitamin E

To evaluate the effect of aspirin treatment upon fetal loss in mice with experimental antiphospholipid syndrome (APLS).. Experimental APLS was induced in pregnant mice by passive transfer of mouse monoclonal anticardiolipin antibody. The mice were treated with high (100 micrograms/d) or low (10 micrograms/d) dose of aspirin, using vitamin C (100 micrograms/d or 10 micrograms/d) as a control. The mice were assessed for the presence of lupus anticoagulants (prolonged aPTT), thrombocytopenia, degree of fetal resorption rate and mean embryo and placental weights.. The mice with APLS had a higher fetal resorption rate (45.7 +/- 12.2% vs 2.5 +/- 0.4%, P < 0.001), reduced placenta mean weight (104 +/- 8 mg vs 169 +/- 7 mg, P < 0.001), prolonged aPTT (94 +/- 14 sec vs 39 +/- 4 sec, P < 0.001), and reduced mean platelet count (597 +/- 186 x 10(3)/mm3 vs 847 +/- 51 x 10(3)/mm3, P < 0.001). The group of mice with APLS, who were treated with low-dose aspirin, had a lower resorption rate (11.1 +/- 9.3% vs 45.7 +/- 12.2%, P < 0.001), a higher placenta mean weight (178 +/- 8 mg vs 104 +/- 8 mg, P < 0.001), a higher mean embryo weight (1042 +/- 134 mg vs 721 +/- 91 mg, P < 0.001), and a lower aPTT (58 +/- 15 sec vs 94 +/- 14 sec, P < 0.001). Mice who were treated with high-dose aspirin also had a lower resorption rate, although not as much as in the low-dose aspirin group (34.2 +/- 12.7% vs 45.7 +/- 12.2%, P < 0.001).. Aspirin, especially in low dose, has a protective effect against obstetrical complications associated with experimental APLS.

Topics: Animals; Antibodies, Monoclonal; Antiphospholipid Syndrome; Ascorbic Acid; Aspirin; Embryo, Mammalian; Female; Fetal Resorption; Male; Mice; Mice, Inbred ICR; Placenta

Administration of ochratoxin A to pregnant rats from 6 to 12 days of gestation period, resulted in complete resorption of fetuses. On histological examination luteal degeneration was observed along with reduction in the weight of corpus luteum (mg/100 mg ovarian tissue) and pituitary gland. The enzyme delta 5-3 beta-hydroxy steroid dehydrogenase (delta 5-3 beta-OHD) and glucose-6-phosphate dehydrogenase were demonstrated histochemically in the ovary of pregnant rats. The activities of the enzymes were suppressed significantly in ochratoxin A treated rats. The same treatment also resulted in an accumulation of cholesterol and ascorbic acid in the ovary. Based on these results, it is suggested that resorption of fetuses in ochratoxin A treated rats may be related with a diminution in ovarian steroidogenesis possibly due to reduction in pituitary gonadotrophin secretion.

Topics: 3-Hydroxysteroid Dehydrogenases; Animals; Ascorbic Acid; Cholesterol; Corpus Luteum; Female; Fetal Death; Fetal Resorption; Glucosephosphate Dehydrogenase; Ochratoxins; Organ Size; Ovary; Pituitary Gland; Pregnancy; Rats