Many of the embryonic malformations arising as a consequence of gene inactivation or of diabetic gestations usually appear with incomplete penetrance10, 12–16, indicating the possible existence of genetic predisposition17–19 or the influence of environmental factors15, 19, 20. A major contributor to embryonic malformations associated to maternal hyperglycaemia is the increased production of reactive oxygen species (ROS) leading to oxidative stress21–23, accompanied by decreased ability of cells to activate antioxidant defence mechanisms24–27. Oxidative stress may contribute considerably to excessive apoptosis during development28, 29, which in turn constitutes an important determinant for the appearance of malformations in developing embryos5, 29.