Lipid peroxidation during ischemia depends on ischemia time in warm ischemia and reperfusion of rat liver

Oxidative Stress in the Ischemic and Non-Ischemic Parts of the Rat Liver after Two-Thirds Ischemia/Reperfusion

“…Although there are some differences in the degree of change of GSH among previous studies, it has been established that total GSH decreased and GSSG increased during I/R. [14][15][16][17][18][19][20] GSH contributes to the recycling of vitamin C, and a decreased level of GSH will affect the content of vitamin C; this has been shown to be sensitive to decrease by the oxidative stress resulting from hepatitis induced by such drugs as carbon tetrachloride, 5) thioacetamide, 4) and D-galactosamine. 6) We followed the change in antioxidative vitamins in the present study, namely water-soluble vitamin C and vitamin E, a hydrophobic antioxidant during I/R injury to the liver.…”

Pyruvate kinase activation and lipoperoxidation after selective hepatic ischemia in Wistar rats

“…These results were expected but this determination was performed so that we could establish and verify the differences detected when analyzing the biochemistry of hepatic tissue. The activation of Kupffer cells and neutrophils caused by ischemia and reperfusion themselves may be mediated by the platelet activating factor, favoring the release of oxygen-derived free radicals and increased calcium influx especially after reperfusion, and reduction of the antioxidant agents superoxide dismutase, catalase and GSH 6,7,8,11,12 , leading to a reduction in NADPH and limiting the peroxide reduction by the antioxidant GSH system and increasing MDA production. Phospholipase activation may cause severe damage to the membrane lipids, changes in mitochondrial permeability and in DNA, proteins, lipids and other macromolecules and oxidative stress progressed during ischemia and triggered the oxidative injury after reperfusion 6,7,8,10,12,13 .…”

“…The factors that most influence the release of these reactive species are ischemia and subsequent reperfusion of the organ during hepatic surgical procedures. The changes observed after the period of ischemia/reperfusion are reflected by disorders in microcirculation, hypotension, elevation of serum aminotransferase and lactate dehydrogenase levels, mitochondrial dysfunction, increased lipoperoxidation, variations of glutathione, changes in cell structure, and cell death 3,4,5,6 . These alterations are the consequence of a complex interaction between ATP consumption, intracellular ion influx, microvascular disorders, release of inflammatory mediators and oxygen-derived free radicals, as well as activation of neutrophils, platelets, Kupffer cells and endothelial cells, which induces the release of proteases and phospholipases that potentially damage the cellular and mitochondrial membranes 1,2,3,4 .…”

“…Glucose 6-phosphate preferentially maintains sufficient blood glucose levels to supply energy to the brain and other tissues, and the glucose that is not immediately utilized is stored as hepatic glycogen. During the process of ischemia/reperfusion, changes occur in these metabolic pathways and the modified energy metabolism may worsen the pre-existing hepatic dysfunction 3,4,5,6,7,8 . Previous studies from our laboratory have shown a change in the metabolic pattern of the liver from the glycogenetic to glycolytic way due to a functional ischemic process during extrahepatic biliary obstruction (A).…”

Isquemia-reperfusão hepática em ratos: efeitos da administração endovenosa da solução salina hipertônica a 7,5% associada a pentoxifilina

“…Surprendentemente, Fukai et al. 25 puderam observar a peroxidação lipídica logo na fase de isquemia, sugerindo a utilização de drogas antioxidantes já neste período.…”