Please use this identifier to cite or link to this item: http://hdl.handle.net/10637/708

Oxidative damage in pregnant diabetic rats and their embryos.

Title: Oxidative damage in pregnant diabetic rats and their embryos.
Authors : Viana Arribas, Marta
Aruoma, Okezie I.
Herrera Castillón, Emilio.
Bonet Serra, Bartolomé
Keywords: Diabetes.Antioxidants.Vitamin E.Teratogenesis.Free radicals.DNA damage.Lipid peroxidation.Protein oxidation.Embryonic malformations.
Abstract: Free radical mechanisms may be involved in the teratogenesis of diabetes. The contribution of oxidative stress in diabetic complications was investigated from the standpoint of oxidative damage to DNA, lipids, and proteins in the livers and embryos of pregnant diabetic rats. Diabetes was induced prior to pregnancy by the administration of streptozotocin (45 mg/kg). Two groups of diabetic rats were studied, one without any supplementation (D) and another treated during pregnancy with vitamin E (150 mg/d by gavage) (D + E). A control group was also included (C). The percentage of malformations in Drats were 44%, higher than the values observed in C (7%) and D + E (12%) animals. D Group rats showed a higher concentration of thiobarbituric acid reactive substances in the mother's liver, however, treatment with vitamin E decreased this by 58%. The levels of protein carbonyls in the liver of C, D, and D + E groups were similar. The "total levels" of the DNA adducts measured, both in liver and embryos C groups were similar to the D groups. Treatment of D groups with vitamin E reduced the levels by 17% in the liver and by 25% in the embryos. In terms of the "total levels" of DNA adducts, the embryos in diabetic pregnancy appear to be under less oxidative stress when compared with the livers of their mothers. Graziewicz et al. (Free Radical Biology & Medicine, 28:75-83, 1999) suggested "that Fapyadenine is a toxic lesion that moderately arrests DNA synthesis depending on the neighboring nucleotide sequence and interactions with the active site of DNA polymerase." Thus the increased levels ofFapyadenine in the diabetic livers and embryos may similarly arrest DNA polymerase, and in the case of this occurring in the embryos, contribute to the congenital malformations. It is now critical to probe the molecular mechanisms of the oxidative stress-associated development of diabetic congenital malformations.
Description: En: Free radical biology and medicine. 2000. n. 29 : 1115-1121 p. 0891-5849
URI: http://hdl.handle.net/10637/708
Rights : http://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
Issue Date: 19-Sep-2000
Center : Universidad San Pablo-CEU
Appears in Collections:Facultad de Farmacia





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