Bulent Ecevit University, School of Medicine, Department of General Surgery, Kozlu, Zonguldak 67600, Turkey.
J Radiat Res. 2013 Jan;54(1):36-44. doi: 10.1093/jrr/rrs073. Epub 2012 Aug 21.
Because radiation-induced cellular damage is attributed primarily to harmful effects of free radicals, molecules with direct free radical scavenging properties are particularly promising as radioprotectors. It has been demonstrated that controlled ozone administration may promote an adaptation to oxidative stress, preventing the damage induced by reactive oxygen species. Thus, we hypothesized that ozone would ameliorate oxidative damage caused by total body irradiation (TBI) with a single dose of 6 Gy in rat liver and ileum tissues. Rats were randomly divided into groups as follows: control group; saline-treated and irradiated (IR) groups; and ozone oxidative preconditioning (OOP) and IR groups. Animals were exposed to TBI after a 5-day intraperitoneal pretreatment with either saline or ozone (1 mg/kg/day). They were decapitated at either 6 h or 72 h after TBI. Plasma, liver and ileum samples were obtained. Serum AST, ALT and TNF-α levels were elevated in the IR groups compared with the control group and were decreased after treatment with OOP. TBI resulted in a significant increase in the levels of MDA in the liver and ileal tissues and a decrease of SOD activities. The results demonstrated that the levels of MDA liver and ileal tissues in irradiated rats that were pretreated with ozone were significantly decreased, while SOD activities were significantly increased. OOP reversed all histopathological alterations induced by irradiation. In conclusion, data obtained from this study indicated that ozone could increase the endogenous antioxidant defense mechanism in rats and there by protect the animals from radiation-induced organ toxicity.
由于辐射诱导的细胞损伤主要归因于自由基的有害影响,因此具有直接清除自由基特性的分子特别有希望成为辐射防护剂。已经证明,受控臭氧给药可能促进对氧化应激的适应,防止由活性氧物质引起的损伤。因此,我们假设臭氧将改善大鼠肝脏和回肠组织中单次 6 Gy 全身照射(TBI)引起的氧化损伤。大鼠随机分为以下几组:对照组;盐水处理和照射(IR)组;臭氧氧化预处理(OOP)和 IR 组。动物在接受 TBI 前 5 天通过腹腔内给予盐水或臭氧(1 mg/kg/天)进行预处理。在 TBI 后 6 小时或 72 小时断头。获得血浆、肝脏和回肠样本。与对照组相比,IR 组的血清 AST、ALT 和 TNF-α 水平升高,经 OOP 治疗后降低。TBI 导致肝脏和回肠组织中 MDA 水平显著升高,SOD 活性降低。结果表明,臭氧预处理照射大鼠的肝脏和回肠组织中 MDA 水平显著降低,而 SOD 活性显著升高。OOP 逆转了照射引起的所有组织病理学改变。总之,这项研究的数据表明,臭氧可以增加大鼠内源性抗氧化防御机制,从而保护动物免受辐射诱导的器官毒性。