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Maleic Vinyl Ether Activation of Murine Macrophages against Lung-metastasizing Tumors¹

Department of Pharmacology [S. E. L., A. E. M.] and MCV/VCU Cancer Center [A. E. M.], Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298

A 15,500 molecular weight fraction of maleic vinyl ether (MVE-2) induced tumoristatic and tumoricidal activity in peritoneal macrophages of BALB/c and C57BL/6 mice following i.p. administration. Growth of B16 melanoma cells in vitro was inhibited up to 85% by MVE-2-activated, but not resident, peritoneal macrophages. In a tritiated thymidine release assay, B16 melanoma cells, and to a lesser extent Madison 109 lung carcinoma cells, were also sensitive to the cytolytic action of MVE-2-activated peritoneal macrophages.

Administration i.v. of MVE-2 resulted in tumoristatic and tumoricidal activity in alveolar macrophages against radiolabeled B16 and Madison 109 lung carcinoma target cells. MVE-2-activated alveolar macrophages significantly inhibited L5178Y lymphoma colony formation following a 48-hr macrophage-tumor cell coincubation.

BALB/c mice bearing the lung-metastasizing Madison 109 lung carcinoma footpad tumor were given MVE-2 i.v., using the same dosing regimen that induced alveolar macrophages to be tumoricidal in vitro. Significant increases in life span were observed, suggesting that the antitumor activity of MVE-2 in this tumor system may be mediated by the activation of alveolar macrophages, with a resulting decrease in metastatic growth in the lung.

¹ This research was supported by USPHS Grant T-32 ES07087 and American Cancer Society Grant IN-105D.

² Present address: Department of Immunology, Michigan Cancer Foundation, 110 E. Warren Ave., Detroit, Mich. 48201. To whom requests for reprints should be addressed.

Received 7/29/80. Accepted 7/10/81.