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

Bakkal, Bekir Hakan | Gultekin F.A. | Guven B. | Turkcu U.O. | Bektas S. | Can M.

Article | 2013 | Brazilian Journal of Medical and Biological Research46 ( 9 ) , pp.789 - 796

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 histopat . . .hological 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 Daha fazlası Daha az

Impact of traumatic rib fractures on pulmonary morbidity and mortality: A multicenter prospective study

Citak, Necati | Pekcolaklar, Atilla | Kok, Abdulaziz | Denizkiran, Ibrahim | Geyik, F. Dogu | Oz, I. Ilker | Evman, Serdar

Conference Object | 2013 | EUROPEAN RESPIRATORY JOURNAL42 , pp.789 - 796

WOS: 000209370402144

The effects of S-nitrosoglutathione on intestinal ischemia reperfusion injury and acute lung injury in rats: Roles of oxidative stress and NF-kB

Turan, İnci | Özaçmak-Sayan, Hale | Özaçmak, Veysel Haktan | Barut, Figen | Özaçmak, I. Diler

Article | 2018 | Tissue and Cell52 , pp.35 - 41

Background: Intestinal ischemia and reperfusion (I/R) induces oxidative stress, inflammatory response, and acute lung injury. S-nitrosoglutathione (GSNO), a nitric oxide donor, has been documented to have protective effects on experimental ischemia models. Aim: The aim of this study was to examine the effect of GSNO on I/R-induced intestine and lung damage and detect the potential mechanisms emphasizing the protective role of GSNO. Methods: Intestinal I/R was induced by occluding the superior mesenteric artery for 30 min followed by reperfusion for 180 min. GSNO was administered intravenously before reperfusion period (0.25 mg/kg). . . .The levels of lipid peroxidation, reduced glutathione, and myeloperoxidase (MPO), histopathological evaluation and immunohistochemical expressions of both nuclear factor KappaB (NF-?B) and inducible nitric oxide (iNOS) in intestine and lung tissues were assessed. Results: Histolopathologic evaluation demonstrated that intestinal I/R induced severe damages in the intestine and the lung tissues. Histopathological scores decreased with GSNO treatment. GSNO treatment reduced lipid peroxidation and MPO levels and inhibited expression of NF-?B and iNOS in the intestine. Conclusion: Our results suggest that GSNO treatment may ameliorate the intestinal and lung injury in rats, at least in part, by inhibiting inflammatory response and oxidative stress. © 2018 Elsevier Lt Daha fazlası Daha az

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