Carcinogenesis Advance Access published online on June 17, 2004
Carcinogenesis, doi:10.1093/carcin/bgh214
© 2004 by Oxford University Press
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1 Food, Nutrition, & Health Program, The University of British Columbia, Vancouver, BC, Canada, V6T 1Z4
* To whom correspondence should be addressed. E-mail: zxu{at}interchange.ubc.ca.
Zinc has been shown to be accumulated in N-methyl-N-nitrosourea-induced rat mammary tumors. Zinc is required for cell proliferation and tumorigenesis is characterized by dysregulation of cell proliferation. An accumulation of zinc in mammary tumors perhaps indicates a need on zinc to sustain tumor growth. Limiting zinc supply by means such as reduced zinc intake should negatively modulate mammary tumorigenesis. Our objective was to determine the effects of zinc status on N-methyl-N-nitrosourea-induced mammary tumorigenesis in sexually mature female rats. Twenty-one-day old Sprague-Dawley rats were assigned to low-zinc (3 mg zinc/kg diet), or adequate-zinc (12 mg zinc/kg diet) ad libitum or pair-fed control group (n = 25-33 rats/group). On day fifty of age, all rats were intraperitoneally injected with N-methyl-N-nitrosourea (50 mg/kg body weight) to induce mammary tumorigenesis. Rats were further maintained on their assigned diet until fourteen weeks post-N-methyl-N-nitrosourea-injection. Total food intake and overall body weight gain were lower in low-zinc rats than in adequate-zinc ad libitum control rats, but were similar to adequate-zinc pair-fed control rats. Plasma zinc concentration was lower in low-zinc rats than in adequate-zinc ad libitum and pair-fed control rats, confirming moderately low-zinc status in low-zinc rats. Tumor incidence (46 versus 84 and 80%; p < 0.05) and tumor multiplicity (0.8 versus 5.0 and 2.6 tumors/rat; p < 0.05), and tumor number (28 versus 123 and 66 tumors) were reduced in low-zinc rats compared with that in adequate-zinc ad libitum and pair-fed control rats, respectively. Tumor latency in low-zinc and adequate-zinc pair-fed control rats was not significantly different, but was longer than in adequate-zinc ad libitum control rats (p<0.05), suggesting that reduced food intake associated with low-zinc intake prolonged tumor latency. Tumor burden and size were not affected by zinc intake. Overall, our observations showed that moderately low-zinc status suppressed N-methyl-N-nitrosourea-induced rat mammary tumorigenesis.
Revised May 26, 2004
Accepted June 10, 2004
MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION
Low zinc intake suppressed N-methyl-N-nitrosourea-induced mammary tumorigenesis in Sprague-Dawley rats
2 UBC Hospital, The University of British Columbia, Vancouver, BC, Canada, V6T 1Z4
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