Abstract
Type II Diabetes model mice (BKS.Cg-+Leprdb/+Leprdb/Jcl, DB mice, 10 weeks old, female) were irradiated with gamma rays at 0.35, 0.70, or 1.2 mGy/hr for 12 weeks. Total superoxide dismutase (SOD) activity decreased both in control and irradiated groups; however, the decrease was less in the irradiated groups, especially in 0.70 mGy/hr group. In this group Mn-SOD activity increased after the 12-week irradiation. A pathological examination of the pancreas revealed that damage to beta cells responsible for the secretion of insulin was much less in the 0.70 mGy/hr group compared to that in the non-irradiated controls. The plasma insulin concentration decreased within the first 4 weeks in all groups, and the level was kept low in the control mice. On the other hand, the insulin level in the irradiated groups showed a tendency to increase. In the 0.70 mGy/hr group the increase was statistically significant after the 12 weeks of irradiation.
These results indicated that the low dose-rate irradiation increase the antioxidative capacity in the pancreas to protect beta cells from oxidative damage, and then to increase the insulin level. This mechanism would lead the mice to the recovery from the disease demonstrated in our previous report.
