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Effects of ozone oxidative preconditioning on radiation-induced organ damage in rats

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 ox...

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Autores principales: Gultekin, Fatma Ayca, Bakkal, Bekir Hakan, Guven, Berrak, Tasdoven, Ilhan, Bektas, Sibel, Can, Murat, Comert, Mustafa
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3534275/
https://www.ncbi.nlm.nih.gov/pubmed/22915786
http://dx.doi.org/10.1093/jrr/rrs073
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author Gultekin, Fatma Ayca
Bakkal, Bekir Hakan
Guven, Berrak
Tasdoven, Ilhan
Bektas, Sibel
Can, Murat
Comert, Mustafa
author_facet Gultekin, Fatma Ayca
Bakkal, Bekir Hakan
Guven, Berrak
Tasdoven, Ilhan
Bektas, Sibel
Can, Murat
Comert, Mustafa
author_sort Gultekin, Fatma Ayca
collection PubMed
description 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.
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spelling pubmed-35342752013-01-03 Effects of ozone oxidative preconditioning on radiation-induced organ damage in rats Gultekin, Fatma Ayca Bakkal, Bekir Hakan Guven, Berrak Tasdoven, Ilhan Bektas, Sibel Can, Murat Comert, Mustafa J Radiat Res Biology 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. Oxford University Press 2013-01 2012-08-21 /pmc/articles/PMC3534275/ /pubmed/22915786 http://dx.doi.org/10.1093/jrr/rrs073 Text en © The Author 2012. Published by Oxford University Press on behalf of The Japan Radiation Research Society and Japanese Society for Therapeutic Radiology and Oncology. http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Biology
Gultekin, Fatma Ayca
Bakkal, Bekir Hakan
Guven, Berrak
Tasdoven, Ilhan
Bektas, Sibel
Can, Murat
Comert, Mustafa
Effects of ozone oxidative preconditioning on radiation-induced organ damage in rats
title Effects of ozone oxidative preconditioning on radiation-induced organ damage in rats
title_full Effects of ozone oxidative preconditioning on radiation-induced organ damage in rats
title_fullStr Effects of ozone oxidative preconditioning on radiation-induced organ damage in rats
title_full_unstemmed Effects of ozone oxidative preconditioning on radiation-induced organ damage in rats
title_short Effects of ozone oxidative preconditioning on radiation-induced organ damage in rats
title_sort effects of ozone oxidative preconditioning on radiation-induced organ damage in rats
topic Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3534275/
https://www.ncbi.nlm.nih.gov/pubmed/22915786
http://dx.doi.org/10.1093/jrr/rrs073
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