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- W2171807788 abstract "Maternal diabetes significantly increases the risk of congenital malformation, a syndrome known as diabetic embryopathy. Nitric oxide (NO), implicated in embryogenesis, has been found elevated in embryos from diabetic rats during organogenesis. The developmental signaling molecules endothelin-1 (ET-1) and 15-deoxy Δ 12,14 prostaglandin J 2 (15dPGJ 2 ) downregulate embryonic NO levels. In the presence of NO and superoxide, formation of the potent oxidant peroxynitrite may occur. Therefore, we investigated peroxynitrite-induced damage, ET-1 and 15dPGJ 2 concentrations, and the capability of ET-1, 15dPGJ 2 and prostaglandin E 2 (PGE 2 ) to regulate NO production in embryos from severely diabetic rats (streptozotocin-induced before pregnancy). We found intense nitrotyrosine immunostaining (an index of peroxynitrite-induced damage) in neural folds, neural tube and developing heart of embryos from diabetic rats ( P < 0.001 vs controls). We also found reduced ET-1 ( P < 0.001) and 15dPGJ 2 ( P < 0.001) concentrations in embryos from diabetic rats when compared with controls. In addition, the inhibitory effect of ET-1, 15dPGJ 2 and PGE 2 on NO production found in control embryos was not observed in embryos from severely diabetic rats. In conclusion, both the demonstrated peroxynitrite-induced damage and the altered levels and function of multiple signaling molecules involved in the regulation of NO production provide supportive evidence of nitrosative stress in diabetic embryopathy." @default.
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- W2171807788 date "2005-11-01" @default.
- W2171807788 modified "2023-10-14" @default.
- W2171807788 title "Peroxynitrites and impaired modulation of nitric oxide concentrations in embryos from diabetic rats during early organogenesis" @default.
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- W2171807788 doi "https://doi.org/10.1530/rep.1.00699" @default.
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