engleski

Antioxidant enzyme status in NOD mouse embryos during diabetic pregnancy

Maternal diabetes increases the rate of congenital malformations in embryos, causing diabetic embryopathy. Although the cellular and molecular mechanisms of diabetic embryopathy are poorly understood, it was shown that maternal hyperglycemia induces oxidative stress in embryos. In this work, we have employed non-obese diabetic (NOD) mouse strain as a model of diabetic embryopathy. In order to assess the incidence of neural tube defects (NTDs), we analyzed external morphology of E (embryonic day) 10, 5 embryos from non-diabetic and alloxan-induced diabetic pregnancies. We found exencephaly as the most common defect, affecting nearly 10 % of all embryos developed under high glucose conditions. Moreover, we analyzed the antioxidant enzyme gene and protein expression in all samples, observing the influence of hyperglycemia only at the translational level.

Antioxidant; NOD; diabetes; NTDs

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