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|Title:||Zinc supplementation prevents cardiomyocyte apoptosis and congenital heart defects in embryos of diabetic mice|
|Citation:||Kumar, S.D., Vijaya, M., Samy, R.P., Dheen, S.T., Ren, M., Watt, F., Kang, Y.J., Bay, B.-H., Tay, S.S.W. (2012-10-15). Zinc supplementation prevents cardiomyocyte apoptosis and congenital heart defects in embryos of diabetic mice. Free Radical Biology and Medicine 53 (8) : 1595-1606. ScholarBank@NUS Repository. https://doi.org/10.1016/j.freeradbiomed.2012.07.008|
|Abstract:||Oxidative stress induced by maternal diabetes plays an important role in the development of cardiac malformations. Zinc (Zn) supplementation of animals and humans has been shown to ameliorate oxidative stress induced by diabetic cardiomyopathy. However, the role of Zn in the prevention of oxidative stress induced by diabetic cardiac embryopathy remains unknown. We analyzed the preventive role of Zn in diabetic cardiac embryopathy by both in vivo and in vitro studies. In vivo study revealed a significant decrease in lipid peroxidation, superoxide ions, and oxidized glutathione and an increase in reduced glutathione, nitric oxide, and superoxide dismutase in the developing heart at embryonic days (E) 13.5 and 15.5 in the Zn-supplemented diabetic group when compared to the diabetic group. In addition, significantly down-regulated protein and mRNA expression of metallothionein (MT) in the developing heart of embryos from diabetic group was rescued by Zn supplement. Further, the nuclear microscopy results showed that trace elements such as phosphorus, calcium, and Zn levels were significantly increased (P|
|Source Title:||Free Radical Biology and Medicine|
|Appears in Collections:||Staff Publications|
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