Physical exercise and redox balance in type 2 diabetics: effects of moderate training on biomarkers of oxidative stress and DNA damage evaluated through comet assay.

Monica Pittaluga,Barbara Tavazzi,Antonio Sgadari,Daniela Caporossi,Paolo Parisi,Ivan Dimauro

doi:10.1155/2015/981242

Abstract

Objective. Hyperglycemia leads to increased production of reactive oxygen species (ROS) in type 2 diabetes, which reduces cellular antioxidant defenses and induces DNA lesions. The aim of this study was to investigate the effects on redox homeostasis and DNA oxidative damage of exercise training in patients with type 2 diabetes compared with nondiabetic individuals. Methods and Results. 12 sedentary type 2 diabetic males (62.1 ± 4.3 yrs) and 12 sedentary healthy males (61.7 ± 3.9 yrs) were exposed to 4-month moderate training, 3 times per week, to evaluate the effect on plasma biomarkers of oxidative stress malondialdehyde and antioxidant status (GSSG, GSH/GSSG, and ascorbic acid) as well as basal and H2O2-induced DNA damage trough alkaline comet assay in peripheral blood lymphocytes. After training, glutathione and ascorbic acid levels increased in both groups, but only in diabetics the malondialdehyde as well as the DNA damage decreased. Conclusion. Our study demonstrates for the first time that moderate exercise training is not only effective in improving the redox homeostasis, through an increase of the endogenous antioxidant defences in healthy as well as in diabetic patients, but also, specifically in diabetic patients, effective in lowering the susceptibility to oxidative DNA damage and the lipid peroxidation levels.

Highlights

Diabetes mellitus (DM) is a metabolic disorder characterized by hyperglycemia resulting from defect either of secretion or action of endogenous insulin [1]
After physical training (PT), the glycemic control resulting significantly improved in diabetic patients, as revealed by the decrease of both basal glycemia (P = 0.023) and glycated haemoglobin (P = 0.01)
Reduced glutathione increased in diabetic patients (DP) (GSH baseline mean value: 30.53 ± 2.05; GSH PT mean value: 31.99 ± 1.67; P < 0.0001) as well as in control group (CG) (GSH baseline mean value: 30.58±2.21; GSH PT mean value: 32.26 ± 2.20; P = 0.015) (Figure 1), but only in DP a significant increase of glutathione ratio (GSH/GSSG) was observed (P = 0.042) (GSH/GSSG baseline values: DP 9.22 ± 2.56; CG 8.53 ± 2.07; GSH/GSSG PT values: DP 10.44 ± 1.82; CG 9.41 ± 1.35) (Figure 2)

Summary

Introduction

Diabetes mellitus (DM) is a metabolic disorder characterized by hyperglycemia resulting from defect either of secretion or action of endogenous insulin [1]. Evidence of depleted antioxidant defences, such as diminished activity of glutathione peroxidase, catalase, and superoxide dismutase, as well as reduced levels of antioxidants in diabetic patients has been widely reported [5,6,7,8,9]. As a consequence, they may accumulate excessively high levels of ROS that lead to acceleration of oxidative damage to cellular proteins, membrane lipids, and DNA [1, 10]. In diabetic patients the amount of DNA damage may be correlated with clinical markers [11]: high concentration of 8-hydroxydeoxyguanosine (8-OHdG), a typical product of DNA oxidation and a sensitive marker of oxidative DNA

Methods

Results

Discussion

Conclusion