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

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.

Rosiglitazone Protects Endothelial Cells From Irradiation-Induced Mitochondrial Dysfunction

“…Despite limited redox defenses, mitochondrial dysfunction and apoptosis were limited after irradiation. This might be due to an adaptive response protecting TICAE-ROSI cells against an overflow of ROS, as was observed in other cells (Belikova et al, 2009) and animals (Bakkal et al, 2013). Therefore, we conclude that rosiglitazone improved mitochondrial function in our model and protects against irradiation-induced apoptosis.…”

Ozone preconditioning attenuates contrast-induced nephropathy in rats

“…The dose of ozone (0.7 mg/kg/d i.p) used in the present study has been previously shown to produce OOP in rat skeletal muscle and intestinal tissues [43,44]. In a recent experimental study, Bakkal et al [14] reported that i.p application of ozone at a dose of 0.7 mg/kg/ d for five consecutive days resulted in amelioration of radiation-induced lung injury via reduction of lipid peroxidation and increment of antioxidant superoxide dismutase activity. Based on this knowledge, we preferred to use a similar regimen to constitute experimental OOP and we observed that it exerts its beneficial effects without causing detectable toxicity.…”

“…Ozone therapy can induce tolerance to ischemic insults and attenuate ischemiaereperfusion (I/R) injury in various tissues including the kidney [11e13]. This phenomenon is known as ozone oxidative preconditioning (OOP) and has been proposed to protect the organs against oxidative stress [14,15].…”

The efficacy of ozone therapy in neonatal rats with hypoxic ischemic brain injury

“…One study reported that intraperitoneally administered ozone decreased the TNF-α level and increased the SOD level in a rat model of experimental peritonitis (4). Bakkal et al repeatedly administered low doses of intraperitoneal ozone to rats with experimentally induced radiation lung injury, and reported a decrease in TNF-α and IL-1β levels, an increase in SOD activity, and a reduction in lung damage (28).…”