<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>The role of the antioxidant defense mechanism in diabetesinduced
anomalies was studied in the Cohen diabetes-sensitive
(CDs) and -resistant (CDr) rats, a genetic model of nutritionally
induced type 2 diabetes mellitus. Embryos, 12.5-day-old, of CDs
and CDr rats fed regular diet (RD) or a diabetogenic high-sucrose
diet (HSD) were monitored for growth retardation and congenital
anomalies. Activity of superoxide dismutase (SOD) and catalaselike
enzymes and levels of ascorbic acid (AA), uric acid (UA), and
dehydroascorbic acid (DHAA) were measured in embryonic homogenates.
When fed RD, CDs rats had a decreased rate of pregnancy,
and an increased embryonic resorption. CDs embryos were
smaller than CDr embryos; 46% were maldeveloped and 7% exhibited
neural tube defects (NTDs). When fed HSD, rate of pregnancy
was reduced, resorption rate was greatly increased (56%;
<italic>P</italic> &lt; .001), 47.6% of the embryos were retrieved without heart
beats, and 27% exhibited NTD. In contrast, all the CDr embryos
were normal when fed RD or HSD. Activity of SOD and catalase
was not different in embryos of CDs and CDr rats fedRD. When fed
HSD, levels of AA were significantly reduced, the ratio DHAA/AA
was significantly increased, and SOD activity was not sufficiently
increased when compared to embryos of CDr. The reduced fertility
of the CDs rats, the growth retardation, and NTD seem to be
genetically determined. Maternal hyperglycemia seems to result in environmentally induced embryonic oxidative stress, resulting in
further embryonic damage.</p>
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Int J Exp Diabetes Res. 2002; 3(4):247-255