| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Nutrition and Metabolism Section, Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research Facility, Frederick, Maryland 21701 [L. A. P., K. S. K., K. L. H.], and Microbiological Associates, Bethesda, Maryland 20816 [M. L. W.]
The effects of calcium and magnesium acetates on the formation of injection site and testicular tumors in male Wistar rats over 2 years following s.c. injections of cadmium chloride (CdCl2) were determined. The rats (25/group) received a single s.c. dose of CdCl2 (0.02 or 0.04 mmol/kg; 0.9% NaCl solutions). Calcium and magnesium acetates were administered as 3% dietary supplements for 2 weeks prior to and 2 weeks after the CdCl2 injection, or as three daily s.c. injections (0.16 mmol calcium acetate per kg, 4 mmol magnesium acetate per kg; 0.9% NaCl solutions) at the same site as CdCl2 on the day before, the day of, and the day after CdCl2 dosing. Control groups were given 0.9% NaCl solution instead of CdCl2 plus s.c. or dietary calcium and magnesium acetates. In rats given injections of CdCl2 alone, the final tumor yields were 33 and 34% of rats at risk at the injection site (mostly fibrosarcomas) and 86 and 85% of rats at risk in the testes (mostly interstitial cell tumors), respectively, for the low- and high-CdCl2 doses. In control rats, the corresponding tumor yields were 0% at the site of 0.9% NaCl solution injection and 30% in the testes. Dietary calcium and magnesium acetates or s.c. calcium acetate did not affect significantly the tumor yields and latent periods. Simultaneous injections of magnesium acetate at the same site completely prevented the development of injection site tumors for both CdCl2 doses but had no effect on the final yields of testicular tumors. CdCl2 injection also caused significant elevation of incidence of the pancreatic islet cell tumors (8.5 versus 2.2%) regardless of any other experimental treatment. These results provide further evidence that the divalent carcinogenic metals may exert their activity through an antagonism with the physiologically essential divalent metals.
1 To whom requests for reprints should be addressed.
2 On sabbatical leave from the Institute of General Chemistry, Technical University of Poznan, Poznan, Poland.
Received 2/23/83. Accepted 7/ 5/83.
This article has been cited by other articles:
![]() |
H. A. Risch Etiology of Pancreatic Cancer, With a Hypothesis Concerning the Role of N-Nitroso Compounds and Excess Gastric Acidity J Natl Cancer Inst, July 2, 2003; 95(13): 948 - 960. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. P. Waalkes, S. Rehm, and M. G. Cherian Repeated Cadmium Exposures Enhance the Malignant Progression of Ensuing Tumors in Rats Toxicol. Sci., March 1, 2000; 54(1): 110 - 120. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. G. Schwartz and I. M. Reis Is Cadmium a Cause of Human Pancreatic Cancer? Cancer Epidemiol. Biomarkers Prev., February 1, 2000; 9(2): 139 - 145. [Abstract] [Full Text] |
||||
![]() |
H. Shimada, T. Funakoshi, and M. P. Waalkes Acute, Nontoxic Cadmium Exposure Inhibits Pancreatic Protease Activities in the Mouse Toxicol. Sci., February 1, 2000; 53(2): 474 - 480. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |