Journal Article

Effect of intact and isoflavone-depleted soy protein on NMU-induced rat mammary tumorigenesis

L.A. Cohen, Z. Zhao, B. Pittman and J.A. Scimeca

in Carcinogenesis

Volume 21, issue 5, pages 929-935
Published in print May 2000 | ISSN: 0143-3334
Published online May 2000 | e-ISSN: 1460-2180 | DOI:
Effect of intact and isoflavone-depleted soy protein on NMU-induced rat mammary tumorigenesis

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Experiments in animal models of carcinogenesis suggest that soy consumption decreases tumor number and incidence. Genistein, an isoflavone which is present in soy at high concentrations, has been considered to be the primary antitumor constituent in soy. In the present study, the N-nitroso-N-methylurea (NMU)-induced mammary tumor model was used as a means to determine whether the chemopreventive effect of soy was attributable specifically to its high content of isoflavones. Five groups of rats (30/group) were fed the following modified AIN-93G diets: group 1, 20% intact soy protein (SP); group 2, 10% SP; group 3, 20% isoflavone-depleted soy protein (IDSP); group 4, 10% IDSP; group 5, the casein-based AIN-93G diet. The SP contained 1.07 and IDSP 0.073 mg genistein/g isolate, respectively. Experimental diets were initiated 1 week prior to NMU administration (at 50 days of age) and continued for another 18 weeks. No significant differences were found among the five groups when assessed in terms of tumor incidence, latency, multiplicity or volume. A trend towards inhibition was observed in both the 20 and 10% SP and IDSP groups when assessed in terms of total tumors/group, tumor volume and latency, but this trend did not achieve statistical significance. The results of this model study do not support the hypothesis that the isoflavone components of soy protein, or soy protein itself, inhibit chemically induced mammary tumor development.

Keywords: DMBA, dimethylbenz[a]anthracene; IDSP, isoflavone-depleted soy protein; NMU, N-nitroso-N-methylurea; SP, intact soy protein.

Journal Article.  6188 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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