Department of Radiological Sciences, College of Applied Medical Sciences-Alkharj, Riyadh, Kingdom of Saudi Arabia.
Inhal Toxicol. 2010 Aug;22(10):797-804. doi: 10.3109/08958370903456629.
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.
本研究旨在探讨周期性高氧训练(PHT)和/或持续暴露于高氧(HP)对肌细胞中超微结构病理变化相关自由基(FR)水平和生物抗氧化潜力(BAP)的影响。30 只成年雄性大鼠随机分为三组:对照组(C)、HP 组或 PHT 组。HP 组大鼠连续 48 小时处于含 100%氧气的环境中,而 PHT 组动物在 3 周的时间内每天进行 3 次每次 30 分钟的 100%氧气呼吸。对 HP 大鼠分离的肌细胞进行超微结构检查显示,肿胀的线粒体伴有嵴内缩和增生,肌原纤维排列紊乱,I 带丢失。对心脏组织上清液的分析也提供了证据,表明 HP 大鼠样本中的 FR 水平明显高于对照组和 PHT 大鼠样本中的值。相比之下,PHT 组大鼠样本中的 BAP 明显高于对照组或 HP 宿主的水平。由于 HP 导致嵴的线粒体病理改变,这意味着诱导心肌氧化应激(MOS)。由于 PHT 增强了 BAP,因此可以得出结论,PHT 可能增强了明显的抗氧化反应,阻止了 FR 的积累。由于预计 PHT 的升高将有助于降低 FR 水平,因此周期性高氧训练似乎可能诱导心脏对潜在的毒性有害反应代谢物形成产生适应性抵抗。