Prevention of diabetes-associated embryopathy by overexpression of the free radical scavenger copper zinc superoxide dismutase in transgenic mouse embryos

Higher than normal levels of the copper zinc superoxide dismutase gene in fetuses may protect them from developing abnormally as a result of diabetes in their mothers. Copper zinc superoxide dismutase is an enzyme that may rid the body of oxygen free radicals, which are overproduced in connection with diabetes mellitus and may cause fetuses to form abnormally. Researchers induced diabetes in mice that were pregnant with embryos either with the human copper zinc superoxide dismutase gene or without it. Mouse embryos with the copper zinc superoxide dismutase gene did not experience growth reductions, had a low rate of malformation and a low rate of fetal death, whereas embryos without the gene were more likely to be small, malformed, or to die before the end of pregnancy.