Role of protein synthesis in the protection conferred by ozone-oxidative-preconditioning in hepatic ischaemia/reperfusion
Hussam H. Ajamieh,1 Jorge Berlanga,2 Nelson Merino,1 Gregorio M. Sá nchez,1 Anna M. Carmona,3
Silvia M. Cepero,4 Atilia Giuliani,5 Lamberto Re6 and Olga S. León1
1 Center for Research and Biological Evaluation (CIEB-IFAL), University of Havana, Havana, Cuba
2 Growth Factor Department, Pharmaceutical Division, Institute of Genetic Engineering and Biotechnology, Havana, Cuba
3 Faculty of Pharmacy, University of Barcelona, Barcelona, Spain
4 Ozone Research Center, Havana, Cuba
5 Department of Chemistry and Medical Biochemistry, University of Milan, Milan, Italy
6 Laboratory of Pharmacological Biotechnology, University of Ancona, Ancona, Italy
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Liver ischaemia/reperfusion, ozone, protein synthesis.
The liver is damaged by sustained ischaemia during liver transplantation, and the reperfusion after ischaemia results in further functional impairment. Ozone oxidative preconditioning (OzoneOP) protected the liver against ischaemia/reperfusion (I/R) injury through different mechanisms. The aim of this study was to investigate the influence of the inhibition of protein synthesis on the protective actions conferred by OzoneOP in hepatic I/R. Rats were treated with cycloheximide (CHX) in order to promote protein synthesis inhibition after OzoneOP treatment. Plasma transaminases, malondialdehyde and 4-hydroxyalkenals and morphological characteristics were measured as an index of hepatocellular damage; Cu/Zn-superoxide dismutase (SOD), Mn-SOD, catalase, total hydroperoxides and glutathione levels as markers of endogenous antioxidant system. OzoneOP increased Mn-SOD isoform and ameliorated mitochondrial damage. CHX abrogated the protection conferred by OzoneOP and decreased Mn-SOD activity. Cellular redox balance disappeared when CHX was introduced. Protein synthesis is involved in the protective mechanisms mediated by OzoneOP. Ozone treatment preserved mitochondrial functions and cellular redox balance.