EFFECT OF TROLOX-C ON HYPOXIA REOXYGENATION-INDUCED INJURY IN ISOLATED-PERFUSED RAT-LIVER/

Livers isolated from 18 hours fasted rats were subjected to N-2 hypoxi a (for 45 min) followed by reoxygenation (for 45 min). The perfusion m edium used was Krebs-Henseleit bicarbonate buffer (KHBB, pH 7.4). Lact ate and alanine were added as gluconeogenic and ureagenic substrates a nd Trolox C was also added to perfusate. Oxygen consumption, lactate d ehydrogenase (LDH), alanine transaminase (ALT), total glutathione, oxi dized glutathione, bile flow, glucose and urea were measured. After hy poxia oxygen consumption significantly dropped but Trolox C had no inf luence on this decrease. ALT and LDH were significantly increased by h ypoxia/reoxygenation. This increase was markedly attenuated in the pre sence of Trolox C. The total glutathione and oxidized glutathione effl ux increased following hypoxia, which were prevented by the treatment of Trolox C. Bile flow rate decreased following hypoxia/reoxygenation but did not continue to decrease in the reoxygenation phase by Trolox C. Following hypoxia/reoxygenation glucose and urea releases decreased . Trolox C had no influence on inhibition of glucose and urea producti on. These results suggest that Trotox C protected the liver cells agai nst hypoxia/reoxygenation injury, yielding further evidence for a caus ative role of oxidative stress in this model.