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HPB Surgery
Volume 8 (1995), Issue 3, Pages 193-199

Clinical and Enzymatic Investigation of Induction of Oxygen Free Radicals by Ischemia and Reperfusion in Human Hepatocellular Carcinoma and Adjacent Liver

From the Second Department of Surgery, Shimane Medical University, Izumo 693, Japan

Copyright © 1995 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Serum concentration of thiobarbituric acid (TBA) reactants in the hepatic vein were measured before and after transient dearterialization of the liver in five human subjects bearing unresectable hepatocellular carcinoma (HCC). During 1 hour of the occlusion of the hepatic artery, change inTBA reactants level was slight. However, the mean value of TBA reactants in 1 hour after the reflow increased to 1.50 ± 0.11 nmol/ml (mean ± S.E.) and was significantly higher (p < 0.05) than those before hepatic dearterialization (1.28 ± 0.11 nmol/ml) and just before the release of occlusion (1.32 ± 0.09 nmol/ml).

Further, two endogeneous scavenger enzymes, superoxide dismutase (SOD) and catalase (CAT), and one of the major sources of oxygen free radicals, xanthine oxidase (XOD) were measured in human untreated HCC and the corresponding adjacent liver tissue. The results demonstrated an increase in SOD in 81.8% (9/11) of HCC, and a decrease in CAT in 72.7% (8/11) of HCC when compared with the corresponding adjacent liver tissue. The mean value of SOD in HCC was significantly higher (66.8 ± 6.5 vs 52.8 ± 3.8 U/mg protein; p < 0.05), and that of CAT was significantly lower (22.6 ± 2.4 vs 36.0 ± 6.1 U/mg protein; p < 0.05) than those in liver tissue. All of nine HCC samples had a significantly lower activity of XOD (6.4 ± 1.9 vs 20.3 ± 3.4 pmol/minute/mg protein; p < 0.01) than the corresponding liver tissue. There was no obvious relation between the content of SOD and CAT in HCC, or in liver tissue.

These data may suggest that oxygen free radicals can be generated in human HCC by ischemia and reperfusion of the tumor- bearing liver. It is also indicated that the antioxidant system of HCC is not always impaired, and that HCC might develop several lines of defence systems against the oxidative attack. A possible strategy of the treatment for liver tumor with oxygen derived free radicals induced by ischemia and reperfusion is hypothized here.