Abstract
The enzyme superoxide dismutase (SOD; superoxide oxidoreductase, EC1. 15. 1.1) is a scavenger of the superoxide radical, a toxic species that has been implicated in DNA damage and protein sulfhydryl oxidation. There are many reports currently available concerning the pathological significance of the superoxide radical on Type 1 diabetes. Therefore, we have studied SOD activities in erythrocytes from non-obese diabetic (NOD) mice, which display a syndrome showing dramatic clinical and pathological features similar to those of Type 1 diabetes in man.
SOD activity in mouse erythrocytes was measured by the nitrite method. This method was 10 times more sensitive than the conventional cytochromec method, and the accuracy and the recovery of SOD activities obtained from this method showed respectable results. Erythrocyte SOD activities in NOD mice were always high in comparison with those in control ICR mice from 3 to 13 weeks of age. SOD activites in NOD mice increased at 6 weeks of age, rapidly decreased around 8 weeks of age, rose again up to 11 weeks of age and then decreased thereafter. Islet cell surface antibodies (ICSA) determined by protin A radioligand assay, were demonstrated at 7 and 11 weeks of age in NOD mice.
These results suggest that the changes in SOD activities between 6 and 9 weeks of age may contribute to the appearance of circulating ICSA. Since changes in the activity of this protective enzyme reflect the amount of the superoxide radical, the latter may play an important role in the pathogenesis of Type 1 diabetes.
