Low-dose radiation induces renal SOD1 expression and activity in type 1 diabetic mice

Abstract

Purpose: Oxidative stress plays a critical role in the pathogenesis of diabetic nephropathy (DN). As an antioxidant, superoxide dismutase (SOD)-1 deficiency exacerbates but SOD1 supplementation prevents diabetes-induced renal damage. Previously, we have demonstrated that repetitive exposure to low-dose radiation (LDR) at 25 mGy significantly prevents DN. Whether this prevention is related to SOD1 expression and activity remains unknown. The aim of the present study was to explore the effects of different methods of LDR treatment on SOD1 expression and activity in the kidneys of diabetic mice.

Materials and methods: C57BL/6J mice were induced with type 1 diabetes using streptozotocin (STZ). Diabetic mice were irradiated with whole-body X-rays at either a single dose of 25 mGy or 75 mGy, or three doses of 25 mGy and then sacrificed at different times. Body weight, blood glucose level, and renal SOD1 expression and activity were measured.

Results: LDR had no impact on the body weights or blood glucose levels of the mice in either the normal or diabetic groups. A single exposure of LDR at 25 mGy did not preserve renal SOD1 expression and activity in diabetic mice, but a single exposure of LDR at 75 mGy or three exposures of LDR at 25 mGy could preserve them.

Conclusion: The stimulation of renal SOD1 expression and activity by a single or cumulative LDR of 75 mGy may be one of the preventive mechanisms of DN observed in the previous study.

Keywords::

• Low-dose radiation
• SOD1
• diabetic nephropathy

Acknowledgements

This study was supported in part by a Young Scientist Award from the National Science Foundation of China (81000294 to CZ), National Science Foundation of China (81370917, to CZ), Research and Development Foundation of Wenzhou Medical University (QTJ13005), National Science Foundation of China (81071920 to WL), Ministry of Education Key Project of Science and Technology (311015 to JC), and Zhejiang Provincial Natural Science Foundation (R2090550 to XL).

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.