Title of article :
Exercise, free radicals, and lipid peroxidation in type 1 diabetes mellitus
Author/Authors :
Gareth W. Davison، نويسنده , , Lindsay George، نويسنده , , Simon K. Jackson، نويسنده , , Ian S. Young، نويسنده , , Bruce Davies، نويسنده , , Damian M. Bailey، نويسنده , , John R. Peters، نويسنده , , Tony Ashton، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2002
Abstract :
Indirect biochemical techniques have solely been used to ascertain whether type 1 diabetes mellitus patients are more susceptible to resting and exercise-induced oxidative stress. To date there is no direct evidence to support the contention that type 1 diabetic patients have increased levels of free radical species. Thus, the aim of this study was to use electron spin resonance (ESR) spectroscopy in conjunction with α-phenyl-tert-butylnitrone (PBN) spin trapping to measure pre- and postexercise free radical concentration in the venous blood of young male patients with type 1 diabetes mellitus (HbA1c = 8.2 ± 1%, n = 12) and healthy matched controls (HbA1c = 5.5 ± 0.2%, n = 13). Supporting measures of lipid peroxidation (malondialdehyde and lipid hydroperoxides), ambient blood glucose and selected antioxidants were also measured. The diabetic patients presented with a comparatively greater concentration of free radicals as measured by ESR and lipid hydroperoxides (LH) compared to the healthy group (p < .05, pooled rest and exercise data), although there was no difference in malondialdehyde (MDA) concentration. α-Tocopherol was comparatively lower in the healthy group (p < .05, pooled rest and exercise data vs. diabetic group) due to a selective decrease during physical exercise (p < .05 vs. rest). The hyperfine coupling constants recorded from the ESR spectra (aNitrogen = 1.37 mT and aβHydrogen = 0.17 mT) are suggestive of either oxygen or carbon-centered species and are consistent with literature values. We suggest that the greater concentration of oxidants seen in the diabetic group may be due to increased glucose autoxidation as a function of this pathology and/or a lower exercise-induced oxidation rate of the major lipid soluble antioxidant α-tocopherol. We suggest that the ESR-detected radicals are secondary species derived from decomposition of LH because these are the major initial reaction products of free radical attack on cell membranes.
Keywords :
ESR , Lipid peroxidation , oxygen free radicals , type 1 diabetes , glucose
Journal title :
Free Radical Biology and Medicine
Journal title :
Free Radical Biology and Medicine