Bakkal B H, Gultekin F A, Guven B, Turkcu U O, Bektas S, Can M
Bulent Ecevit University, Department of Radiation Oncology, School of Medicine, KozluZonguldak, Turkey.
Braz J Med Biol Res. 2013 Sep;46(9):789-96. doi: 10.1590/1414-431X20132856. Epub 2013 Sep 27.
Ionizing radiation causes its biological effects mainly through oxidative damage induced by reactive oxygen species. Previous studies showed that ozone oxidative preconditioning attenuated pathophysiological events mediated by reactive oxygen species. As inhalation of ozone induces lung injury, the aim of this study was to examine whether ozone oxidative preconditioning potentiates or attenuates the effects of irradiation on the lung. Rats were subjected to total body irradiation, with or without treatment with ozone oxidative preconditioning (0.72 mg/kg). Serum proinflammatory cytokine levels, oxidative damage markers, and histopathological analysis were compared at 6 and 72 h after total body irradiation. Irradiation significantly increased lung malondialdehyde levels as an end-product of lipoperoxidation. Irradiation also significantly decreased lung superoxide dismutase activity, which is an indicator of the generation of oxidative stress and an early protective response to oxidative damage. Ozone oxidative preconditioning plus irradiation significantly decreased malondialdehyde levels and increased the activity of superoxide dismutase, which might indicate protection of the lung from radiation-induced lung injury. Serum tumor necrosis factor alpha and interleukin-1 beta levels, which increased significantly following total body irradiation, were decreased with ozone oxidative preconditioning. Moreover, ozone oxidative preconditioning was able to ameliorate radiation-induced lung injury assessed by histopathological evaluation. In conclusion, ozone oxidative preconditioning, repeated low-dose intraperitoneal administration of ozone, did not exacerbate radiation-induced lung injury, and, on the contrary, it provided protection against radiation-induced lung damage.
电离辐射主要通过活性氧诱导的氧化损伤产生其生物学效应。先前的研究表明，臭氧氧化预处理可减轻由活性氧介导的病理生理事件。由于吸入臭氧会导致肺损伤，本研究的目的是检查臭氧氧化预处理是增强还是减轻辐射对肺的影响。将大鼠进行全身照射，有或没有臭氧氧化预处理（0.72mg/kg）。在全身照射后6小时和72小时比较血清促炎细胞因子水平、氧化损伤标志物和组织病理学分析。照射显著增加了作为脂质过氧化终产物的肺丙二醛水平。照射还显著降低了肺超氧化物歧化酶活性，这是氧化应激产生的指标以及对氧化损伤的早期保护反应。臭氧氧化预处理加照射显著降低了丙二醛水平并增加了超氧化物歧化酶的活性，这可能表明对肺有保护作用，使其免受辐射诱导的肺损伤。全身照射后显著升高的血清肿瘤坏死因子α和白细胞介素-1β水平，经臭氧氧化预处理后降低。此外，通过组织病理学评估，臭氧氧化预处理能够改善辐射诱导的肺损伤。总之，臭氧氧化预处理，即重复低剂量腹腔注射臭氧，并不能加重辐射诱导的肺损伤，相反，它提供了针对辐射诱导的肺损伤的保护作用。
