Pregnancy in diabetic females causes delay in early stages of
   embryonic growth and development and higher incidence of congenital malformations and spontaneous miscarriage compared with those of non-diabetic conditions. High glucosis tratogenicity seems to be related to reduction of Nitric Oxide production (NO) in hyperglycemic condition. The goal of present work was study of nitric oxid role in control of mouse preimplantation embryonic defects in high glucosis media.

          In order to test above hypothesis, 2-cell stage embryos of normal mice were cultured with high concentration of glucose (30mM) and different concentrations of L-arginine (5,10,20 mM) or L-NAME (An antagonist of L-arginine). After 96h culture, the morphology of embryos was assessed by an inverted microscope then blastocysts were stained by TUNEL. After TUNEL the total cell number and apoptotic cells were counted by use a Fluorescence microscope. Finally the amount of nitrite in the media was assayed by Greiss method. 

          The results indicated that high glucose decreases the blastocyst formation and Nitric Oxide production and increases their apoptotic index, but 10-20mM L-arginine significantly increases the developmental potential and nitric oxide production and significantly decreases apoptosis. On the contrary L-NAME significantly inhibits the development of pre-implantation
   embryos .

          It seems that during pregnancy supplementation of high glucose media with L-arginine increases Nitric Oxide production and prevents high glucosis embryotoxicity.