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Antitumor Effect of Ischemia-Reperfusion Injury Induced by Transient Embolization

First Department of Medicine, Kyoto Prefectural University of Medicine, Kamigyou-ku, Kyoto 602, Japan [T. Y., S. K., H. O., S. I., S. N., T. K., Y. N., M. K.] and Research Center for Advanced Science and Technology, The University of Tokyo, 4-6-1, Komaba, Meguro-ku, Tokyo 153, Japan [T. Y.]

The effect of ischemia-reperfusion, induced by the transient embolic agent degradable starch microspheres (DSMs) on tumor tissue was investigated from the standpoint of active oxygen species. Rabbits with VX2 carcinoma received regional infusion of DSMs by transcatheter angiography, and it was confirmed that DSMs occluded tumor vessels. Blood flow in the tumors decreased rapidly immediately after the DSM treatment and returned to the original level within 40 min. The size of tumors did not change after a single infusion of DSM, while five repeated DSM treatments led to a significant reduction in tumor size. This reduction in tumor size was prevented by the treatment of rabbits with superoxide dismutase and catalase, indicating that the generation of active oxygen species in the tumor was involved in the mechanism of action of DSMs. Thiobarbituric acid-reactive substances also increased in the tumors after DSM infusion, and this increase was also inhibited by treatment with superoxide dismutase and catalase.

In conclusion, the antitumor effect of the transient embolic agent DSM is secondary to the phenomenon of ischemia-reperfusion injury. In addition, active oxygen species and lipid peroxidation are passible causes of ischemia-reperfusion injury.

¹ To whom requests for reprints should be addressed.

Received 7/15/94. Accepted 8/18/94.