In their letter (17), Chander M. Pathak and Krishan K. Khanduja commended the findings of our paper (27). We are grateful to them for highlighting the clinical relevance and important implications of our research. However, two issues require clarification.First, we did not simultaneously investigate the temporal long-term impact of whole body low-dose radiation (WB-LDR) on both pancreatic and renal tissue in diabetic animals (27). One reason is that we focused on the preventive effect of WB-LDR on diabetic kidney. With this goal in mind, all animals in the study were treated with multiple low doses of streptozotocin (STZ), which destroyed pancreatic -cells before WB-LDR was given. However, studies by others suggest that WB-LDR at 0.5 Gy gamma rays, administered either before alloxan-induced diabetes or in NOD mice with spontaneously developed diabetes, leads to upregulation of pancreatic antioxidants (22,23). There was also a study indicating that chronic exposure of type 2 diabetic db/db mice to LDR significantly upregulated pancreatic antioxidants along with reduction of glucose levels (24). These findings suggest that WB-LDR can induce pancreatic antioxidant upregulation, resulting in certain preventive effects on diabetic complications, but this hypothesis has yet to be specifically tested. We recently demonstrated that STZ-induced diabetes significantly reduces systemic (plasma) and testicular antioxidants (catalase and superoxide dismutase) and then showed that repeated WB-LDR (25 or 50 mGy X-rays) in posthyperglycemic diabetic rats significantly prevented reduction of diabetes-induced systemic and testicular antioxidants and also prevented diabetes-induced testicular cell death and oxidative damage (28).The second issue is that we did not explore the optimal conditions for WB-LDR to effectively protect the kidney from diabetes. The authors pointed out that the application of moderate doses (between 3 and 6 Gy) for therapeutic purposes to diabetic patients appear to be unacceptable to the scientific community, since with application of higher radiation doses acute toxic effects and potentially late long-term effects are expected. Unlike high and middle doses of ionizing radiation, LDR induces few detrimental effects and significantly stimulates cellular metabolism and enhances cell defense function, which is known as hormesis and adaptive response (2, 3, 12, 25). The hormetic and adaptive response includes the stimulation of DNA, RNA, and protein synthesis as well as DNA repair activity, the increase in cellular antioxidant capacity, the prolongation of life span, and the activation of immune functions. Whether LDR can be considered as an alternative approach to preventing diabetes and diabetic complications has been questioned (25). In the study under discussion here, however, we demonstrated that accumulated dose 0.175 Gy at week 2 and 0.35 Gy at week 4 can significantly protect the kidney from diabetes-induced inflammation, dysfunction, and oxidative damage. At higher radiation doses (0.70 Gy at week 8 ...