No evidence of intracellular oxidative stress during ischemia-reperfusion damage in rat liver in vivo.
The role of the intracellular generation of reactive oxygen species in the pathogenesis of ischemia-reperfusion damage of the liver was investigated in two in vivo rat models. Global hepatic ischemia was produced in the left and median lobes for 90 min followed by 60 min reperfusion to the total organ (model A) or only to the ischemic lobes (model B). Although both regimens caused significant rises in serum transaminases, this rise was higher in model B. In neither model was intracellular hydrogen peroxide production nor increased glutathione disulfide in bile found. The activities of various antioxidant enzymes were not affected by ischemia or ischemia-reperfusion. In conclusion, oxygen-free radicals are unlikely to be produced in the cells of rat liver during ischemia-reperfusion.
Villa
P
P
C.N.R. Center of Cytopharmacology, Department of Pharmacology, Milan, Italy.
Carugo
C
C
Guaitani
A
A
D000410:Alanine Transaminase / Q000097:blood; D000640:Amitrole / Q000494:pharmacology; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D002374:Catalase / Q000378:metabolism; D007511:Ischemia / Q000378:metabolism*; D008099:Liver / Q000098:blood supply* / Q000187:drug effects / Q000378:metabolism; D008297:Male; D009582:Nitrofurantoin / Q000494:pharmacology; D010084:Oxidation-Reduction; D051381:Rats; D015427:Reperfusion Injury / Q000201:enzymology / Q000378:metabolism*
D009582:Nitrofurantoin; D002374:Catalase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D000640:Amitrole