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[Cancer Research 43, 73-77, January 1, 1983]
© 1983 American Association for Cancer Research

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Effects of Amiloride on Tumor Growth and Intracellular Element Content of Tumor Cells in Vivo1

R. L. Sparks2, T. B. Pool, N. K. R. Smith and I. L. Cameron3

Department of Anatomy, The University of Texas Health Science Center at San Antonio, San Antonio, Texas 78284

The effects of amiloride, a reported inhibitor of serum-stimulated sodium influx, were tested on tumor growth, tumor cell proliferation, and intracellular element content of cancer cells in vivo. We have shown previously that cancer cells have high intranuclear levels of sodium compared to those of their normal counterpart cells and have postulated that such a high level of sodium may be involved in the cancer state. We now report that amiloride, when given in a series of injections, inhibited both H6 hepatoma and DMA/J mammary adenocarcinoma growth in vivo in a dose-dependent fashion and that 3 injections of amiloride at a dose of 1.0 µg/g body weight into mice bearing H6 hepatomas resulted in a significant decrease in the intranuclear content of sodium but not the content of magnesium, phosphorus, sulfur, chlorine, or potassium as measured by electron probe X-ray microanalysis in the H6 hepatoma cells. Amiloride at dosages as low as 1.0 µg/g body weight per injection also inhibited tumor cell proliferation as measured by the tritated thymidine autoradiography labeling index. Amiloride caused no changes in the mean profile diameters of metaphase or interphase H6 hepatoma or DMA/J mammary adenocarcinoma cells, suggesting that the action of amiloride on tumor growth was not due to cell volume changes. These data show that amiloride both inhibited tumor growth and decreased the proliferation of the tumor cells in the H6 hepatomas which was correlated with a decreased intranuclear sodium content.

1 Supported by Grant PCM 804084 from The United States National Science Foundation.

2 Present address: Division of Biophysics, School of Hygiene and Public Health, The Johns Hopkins University, Baltimore, Md. 21205.

3 To whom requests for reprints should be addressed, at Department of Anatomy, The University of Texas Health Science Center at San Antonio, San Antonio, Texas 78284.

Received 1/ 8/82. Accepted 10/11/82.




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C. Boyd and A. Naray-Fejes-Toth
Steroid-Mediated Regulation of the Epithelial Sodium Channel Subunits in Mammary Epithelial Cells
Endocrinology, August 1, 2007; 148(8): 3958 - 3967.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
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Molecular Cancer Research Cancer Prevention Research
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Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1983 by the American Association for Cancer Research.