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Vol. 289, Issue 1, 559-564, April 1999
Callerio Foundation, Institutes of Biological Research (A.B., R.G.,
G.S.) and Departments of
Biomedical Sciences (V.S., A.F., G.S.) and
Chemical Sciences (E.A., G.M.), University of Trieste, Trieste, Italy
The effects of NAMI-A (imidazolium
trans-imidazoledimethyl sulfoxide-tetrachlororuthenate)
are compared with cisplatin on tumor cells cultured in vitro at doses
of 1 to 100 µM and on tumor metastases in vivo at maximum tolerated
doses. Using mouse tumors that metastasize to the lungs, NAMI-A given
i.p. for 6 consecutive days at 35 mg/kg/day, was effective
independently of the tumor line being treated and of the stage of
metastasis growth. Conversely, cisplatin (2 mg/kg/day for 6 days) was
as effective as NAMI-A on MCa mammary carcinoma and TS/A
adenocarcinoma and less effective than NAMI-A on Lewis lung carcinoma.
Cisplatin reduced body weight gain and spleen weight during treatment
and was much more toxic than NAMI-A on liver sinusoids, kidney tubules,
and lung epithelium. In vitro NAMI-A caused a transient cell cycle
arrest of tumor cells in the premitotic G2/M phase, whereas
cisplatin caused a progressive dose-dependent disruption of cell cycle
phases. Correspondingly, NAMI-A did not modify cell growth, whereas
cisplatin caused a dose-dependent reduction of cell proliferation, as
determined by sulforhodamine B test. Thus, NAMI-A, unlike cisplatin, is
a potent agent for the treatment of solid tumor metastases as well as
when these tumor lesions are in an advanced stage of growth. NAMI-A is
endowed with a mechanism of action unrelated to direct tumor cell
cytotoxicity, and such mechanism of action is responsible for a reduced
host toxicity.
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