Keywords: type I diabetes, low dose X-rays, ROS related diseases, superoxide dismutase, apoptosis, non-obese diabetic, low radiation, urine glucose level, diabetes suppression, low dose irradiation, antioxidant defence mechanisms, pancreas, reactive oxygen species
Suppressive effect of low-dose X-irradiation on type I diabetes non-obese diabetic (NOD) mice
We examined the effect of X-irradiation (0, 0.25, 0.5 or 1.0 Gy) on the onset of the type I diabetes (insulin dependent diabetes mellitus) in non-obese diabetic (NOD) mice. NOD mice are characterised by a progressive loss of insulin-producing β-cells in the pancreas by autoimmune mechanisms. The destruction of β-cells is known to be due to apoptosis induced by oxidative stress caused by ROS. In non-irradiated NOD mice, an elevation of the urine glucose level was first detected at 15 weeks of age. When the mice were irradiated with 0.5 Gy of X-rays (300 kVp) at 12 weeks of age, the onset of disease delayed to the 22nd week. When irradiated at 13th or 14th week, the suppression was much less effective. One week after the 0.5 Gy irradiation, an increase in the specific activity of superoxide dismutase (SOD) in pancreas was observed. The level was twice as much as that in the non-irradiated control mice. In the dose range we examined 0.5 Gy gave the most effective suppression of the diabetes. The same dose was also most effective in increasing the SOD level. Furthermore, detection of apoptotic cells by TUNEL method revealed far fewer incidences of apoptosis in pancreas of the irradiated mice than in non-irradiated NOD mice. The results suggest that the low dose irradiation delayed the onset of type I diabetes in NOD mice by suppressing apoptotic cell death in pancreas, probably through enhancing antioxidant defence mechanisms.