Role of active oxygen species and lipid peroxidation in liver injury induced by ischemia-reperfusion

• Published in: Nippon Shōkakibyō Gakkai zasshi Vol. 87; no. 2; p. 199
• Main Authors: Yoshikawa, T, Oyamada, H, Ichikawa, H, Naito, Y, Ueda, S, Tainaka, K, Takemura, T, Tanigawa, T, Sugino, S, Kondo, M
• Format: Journal Article
• Language: Japanese
• Published: Japan 1990
• Subjects: Animals; Catalase - pharmacology; Ischemia - metabolism; Ischemia - physiopathology; Lipid Peroxidation - drug effects; Liver - blood supply; Liver - metabolism; Liver Circulation - drug effects; Male; Oxygen - physiology; Rats; Rats, Inbred Strains; Reperfusion; Superoxide Dismutase - pharmacology; Thiobarbiturates - pharmacology
• ISSN: 0446-6586
• DOI: 10.11405/nisshoshi1964.87.199

The role of superoxide and lipid peroxidation in liver injury induced by ischemia-reperfusion was investigated in rats. Ischemic condition of the liver was created by applying small clamps to the right branch of portal vein and the right hepatic artery for 15 min. Clamping of hepatic artery and portal vein could decrease the hepatic blood flow to about 30% of that measured before the clamping. Levels of serum GPT and thiobarbituric acid (TBA) reactive substances in the liver tissue were significantly increased 30 min after the reperfusion following 15 min of ischemia. The increase in serum GPT and TBA reactants in the liver tissue was significantly inhibited by the treatment with superoxide dismutase combined with catalase. The treatment with allopurinol significantly inhibited the elevation of serum GPT levels and showed a tendency to inhibit the increase in TBA reactants in liver tissue. These results suggest that active oxygen species and lipid peroxidation may play an important role in the pathogenesis of ischemia-reperfusion injury in the liver, and hypoxanthine-xanthine oxidase system may be one of the main sources of active oxygen species.