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Abstract
OBJECTIVES: It has recently been suggested that oxygen free radicals are involved in the high
incidence of fetal dysmorphogenesis that is associated with diabetic pregnancies.
The purpose of the current investigation was to study the effect of copper zinc superoxide
dismutase, a free radical scavenging enzyme, on the prevention of diabetes-associated
embryopathy in mice.
STUDY DESIGN: Mice used in this study were either transgenic, bearing the human copper zinc superoxide
dismutase gene, or nontransgenic controls. Diabetes was generated by streptozotocin
administration on days 6 and 7 of gestation. Hyperglycemia developed on day 8 and
was maintained through day 10 (critical period of organogenesis). On day 10 fetuses
were examined for external anomalies, and their crown-rump lengths and deoxyribonucleic
acid content were determined. RESULTS: Induction of maternal diabetes produced a significant reduction in mean crown-rump
length of control embryos (4.48 ± 0.7 mm vs 3.65 ± 0.6 mm, p = 0.0001), whereas trangenic embryos were not affected (4.72 ± 0.6 mm vs 4.45 ± 0.8
mm, p > 0.05). After induction of diabetes fetal loss and malformation rates were significantly
higher in control embryos (6.0% vs 23.8% and 8.4% vs 16.5%, respectively). Transgenic
embryos were practically unaffected by diabetes and showed fetal loss and malformation
rates of 5.9% and 4.4%, respectively, after induction of diabetes.
CONCLUSIONS: Elevated levels of copper zinc superoxide dismutase, a key enzyme in the metabolism
of free oxygen radicals, elicit a protective effect against diabetes-associated embryopathy.
Keywords
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Article Info
Footnotes
☆Presented at the Fifteenth Annual Meeting of the Society of Perinatal Obstetricians, Atlanta, Georgia, January 23–28, 1995.
Identification
Copyright
© 1995 Published by Elsevier Inc.