Open AccessRole of protein synthesis in the protection conferred by ozone‐oxidative‐preconditioning in hepatic ischaemia/reperfusion
Author(s) -
Ajamieh Hussam H.,
Berlanga Jorge,
Merino Nelson,
Sánchez Gregorio M.,
Carmona Anna M.,
Cepero Silvia M.,
Giuliani Atilia,
Re Lamberto,
León Olga S.
Publication year - 2005
Publication title -
transplant international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.998
H-Index - 82
eISSN - 1432-2277
pISSN - 0934-0874
DOI - 10.1111/j.1432-2277.2005.00101.x
Subject(s) - superoxide dismutase , oxidative stress , malondialdehyde , catalase , cycloheximide , pharmacology , reperfusion injury , ischemia , biochemistry , antioxidant , medicine , liver transplantation , transplantation , chemistry , protein biosynthesis
Summary 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 OzonoOP 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.