Table of Contents
Metal-Based Drugs
Volume 2, Issue 4, Pages 195-199

Efficacy of 5-FU Combined to Na[trans-RuCl4(DMSO)Im] , A Novel Selective Antimetastatic Agent, on the Survival Time of Mice With P388 Leukemia, P388/DDP subline and MCa Mammary Carcinoma

1Department of General Pathology and Oncology, University of Bari, Italy
2Institute of Pharmacology and Pharmacognosy, University of Trieste, Trieste, Italy
3Department of Chemical Sciences, University of Trieste, Trieste, Italy
4Fondazione Callerio, Institutes of Biological Research, Via A. Fleming, 22 - 31, Trieste 1 - 34127, Italy

Received 14 February 1995; Accepted 1 March 1995

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.


The combinational treatment between the selective antimetastatic agent, sodium-trans-rutheniumtetrachloridedimethylsulfoxideimidazole, Na[trans-RuCl4(DMSO)Im], and the cytotoxic drug 5-fluorouracil (5-FU) on primary tumor growth and on the survival time of experimental tumors results in an effect significantly greater than that of each single agent used alone either with the solid metastasizing MCa mammary carcinoma of the CBA mouse or with the lymphocytic leukemia P388 and its platinum resistant P388/DDP subline. Thus the inorganic compound Na[trans-RuCl4(DMSO)Im], known for its potent and selective antimetastatic effects, positively interacts with the antitumor action of an organic anticancer agent such as 5-FU on both a solid metastasizing tumor and a tumor of lymphoproliferative type. In particular, the effects of the combinational treatment on the survival time of tumor bearing mice seem to be related to the selective antimetastatic activity of the ruthenium complex that joins the potent cytotoxicity of 5-FU for the tumor. Moreover, these data show that Na[trans-RuCl4(DMSO)Im] is almost as effective on the subline of P388 made resistant to cisplatin as it was on the parental line.