title: Exercise, free radicals, and lipid peroxidation in type 1 diabetes mellitus.
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 alpha-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 (HbA(1c) = 8.2 +/- 1%, n = 12) and healthy matched controls (HbA(1c) = 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. alpha-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 (a(Nitrogen) = 1.37 mT and abeta(Hydrogen) = 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 alpha-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.
authors.affiliation: School of Applied Medical Sciences and Sports Studies, University of Ulster Jordanstown, Belfast, UK.
authors.forename: Gareth W
authors.initials: GW
authors.lastname: Davison
authors.forename: Lindsay
authors.initials: L
authors.lastname: George
authors.forename: Simon K
authors.initials: SK
authors.lastname: Jackson
authors.forename: Ian S
authors.initials: IS
authors.lastname: Young
authors.forename: Bruce
authors.initials: B
authors.lastname: Davies
authors.forename: Damian M
authors.initials: DM
authors.lastname: Bailey
authors.forename: John R
authors.initials: JR
authors.lastname: Peters
authors.forename: Tony
authors.initials: T
authors.lastname: Ashton
mesh_terms: D000293:Adolescent; D000328:Adult; D001205:Ascorbic Acid / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D016022:Case-Control Studies; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000378:metabolism*; D004578:Electron Spin Resonance Spectroscopy; D015444:Exercise; D005609:Free Radicals; D006454:Hemoglobins / Q000737:chemistry; D006801:Humans; D015227:Lipid Peroxidation; D008054:Lipid Peroxides; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D018384:Oxidative Stress; D010100:Oxygen / Q000378:metabolism; D024502:alpha-Tocopherol / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D005609:Free Radicals; D006454:Hemoglobins; D008054:Lipid Peroxides; D008315:Malondialdehyde; D024502:alpha-Tocopherol; D001205:Ascorbic Acid; D010100:Oxygen