Effect of ozone oxidative preconditioning in preventing early radiation-induced lung injury in rats

B.H Bakkal,S Bektas,M Can,F.A Gultekin,U.O Turkcu,B Guven

doi:10.1590/1414-431x20132856

B.H Bakkal, S Bektas + Show 4 more

Open Access

https://doi.org/10.1590/1414-431x20132856

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Abstract

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.

Highlights

Whole body exposure to ionizing radiation (IR) may trigger in humans and animals multiple organ dysfunction directly related to an increase in cellular oxidative stress due to overproduction of reactive oxidative species (ROS) from molecular ionization [1,2]
Biochemical analysis enzyme-linked immunosorbent assay (ELISA) analysis indicated that animals in the irradiated group had significantly increased serum tumor necrosis factor alpha (TNF-a) and IL-1b at both 6 and 72 h post-irradiation compared to control animals (P=0.001)
Studies have so far shown that ozone therapy appears useful in diseases including peritonitis, infected wounds, chronic skin ulcers, initial gangrene, burns, and advanced ischemic diseases [15]

Summary

Introduction

Whole body exposure to ionizing radiation (IR) may trigger in humans and animals multiple organ dysfunction directly related to an increase in cellular oxidative stress due to overproduction of reactive oxidative species (ROS) from molecular ionization [1,2]. Any agent exhibiting antioxidant effects can help protect cells from radiation toxicity. Ozone administration has been shown to exert a protective effect against liver damage induced by carbon tetrachloride and against renal ischemic-reperfusion injury by an oxidative preconditioning mechanism that stimulates antioxidant endogenous systems and modulates nitric oxide production [6]. The term ‘‘ozone oxidative preconditioning’’ (OOP) refers to the administration of ozone at repeated nontoxic doses that provide an adaptation to oxidative stress. Adaptation occurs through the induction of enzymes or by activating

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