Effects of exposure of rats to periodic versus continuous hyperoxia on antioxidant potentials and free radical production in relation to ultrastructural changes in myocardial cells.
The purpose of the present study was to examine the effects of periodic hyperoxia training (PHT) and/or continuous exposure to hyperoxia (HP) on free radical (FR) levels and biological antioxidant potentials (BAPs) in relation to ultrastructural pathological changes in myocytes. Thirty adult male rats were randomly assigned to three groups: control (C), HP, or PHT. HP rats were continuously subjected to atmospheres containing 100% O2 for 48 h, whereas PHT animals breathed 100% O2 for 30-min periods three times daily over a 3-week period. Ultrastructural examination of isolated myocytes from the HP rats showed that swelled mitochondria with constricted and proliferated cristae of the inner membrane were associated with disarrangement of myofibrils as well as the loss of I-banding. Heart tissue supernatant analyses also provided evidence of significantly higher FR levels in samples from the HP rats as compared with values noted with materials from control and PHT rats. In contrast, BAP was significantly higher in the samples from rats in the PHT group as compared levels associated with the control or the HP hosts. As HP resulted in mitochondrial pathological alterations in the cristae, this implied the induction of a myocardium oxidative stress (MOS). As PHT enhanced BAP, it may be concluded that PHT likely enhances an apparent antioxidant response that did not permit FR to build up. Because PHT elevations would be expected to help lower FR levels, it would seem that periodic hyperoxia training might induce an adaptive resistance in the heart against the formation of potentially toxicologically deleterious reactive metabolite species.
Haffor
Al-Said A
AS
Department of Radiological Sciences, College of Applied Medical Sciences-Alkharj, Riyadh, Kingdom of Saudi Arabia. ahaffor@ksu.edu.sa
Alttas
Omar S
OS
D000222:Adaptation, Physiological; D000818:Animals; D001835:Body Weight; D005609:Free Radicals / Q000378:metabolism*; D018496:Hyperoxia / Q000378:metabolism*; D008297:Male; D046529:Microscopy, Electron, Transmission; D008929:Mitochondria, Heart / Q000378:metabolism / Q000648:ultrastructure; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000648:ultrastructure; D009210:Myofibrils / Q000648:ultrastructure; D018384:Oxidative Stress / Q000502:physiology*; D010100:Oxygen / Q000008:administration & dosage; D010507:Periodicity; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism
D005609:Free Radicals; D017382:Reactive Oxygen Species; D010100:Oxygen