Abstract

Induction of hormesis and adaptive response by low-dose radiation (LDR) has been extensively indicated. Adaptive response induced by LDR was not only resistant to damage caused by a subsequently high-dose radiation, but also cross-resistant to other non-radiation challenges, such as chemicals. Mechanisms by which LDR induces the preventive effect on radiation- or chemical-induced tissue damage include induced or up-regulated expression of protective proteins, such as heat shock proteins and antioxidants. Since oxidative damage to tissues is a major pathogenesis of many human diseases including diabetes, this review will summarize the available data with an emphasis of the preventive effect of LDR on the development of diabetes and the therapeutic effect of LDR on diabetic cardiovascular complications. The available data indicated that pre-exposure of mice to LDR reduced the incidence of alloxan-induced diabetes, and also delayed the onset of hyperglycaemia in diabetes-prone non-obese diabetic mice. Experiments with animals indicated the effectively therapeutic effect of low-intensity or power laser (LIL or LPL) radiation on skin wound healing, which has stimulated clinical use of LIL to cure skin ulcer in diabetic patients. Mechanisms by which LDR prevents diabetes, though are unclear now, may include the induction of pancreatic antioxidants to prevent beta cell from oxidative damage and immunomodulation to preserve pancreatic function. For LIL therapeutic effect on diabetic wound healing, mechanisms may include its antioxidant action, immunomodulation, cell proliferation stimulation as well as improvement of systemic and wound-regional microcirculation. Therefore, although only a few studies indicating LDR prevention of the development of diabetes, many studies have demonstrated LDR, specifically LIL, therapeutic effectiveness of diabetic wound healing. These preliminary results are really encouraging for us to further pursue the clinical implication of LDT to diabetes-related areas.

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