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Dairy Proteins Protect against Dimethylhydrazine-Induced Intestinal Cancers in Rats^1,2,

CSIRO Division of Human Nutrition, Adelaide, South Australia, 5000 ^* CSIRO Division of Food Science and Technology, Melboume Laboratory, Highett, Victoria 3190, Australia

The impact of different dietary protein sources (whey, casein, soybean, red meat) on the incidence, burden and mass index of intestinal tumors induced by dimethylhydrazine in male Sprague-Dawley rats was assessed. A purified diet (based on AIN-76A) with a fat concentration of 20 g/100 g and other proteins substituted for casein (20 g/100 g) was used. Whey and casein diets were more protective against the development of intestinal tumors than were the red meat or soybean diets, as evidenced by a reduced incidence of rats affected (P = 0.15), fewer tumors per treatment group (burden, P < 0.005), and a reduced pooled area of tumors (tumor mass index) that formed (P = 0.39). Intracellular concentration of glutathione, an antioxidant and anticarcinogenic tripeptide, measured in liver, was greatest in whey protein- and casein-fed rats and lowest in soybean-fed animals (P < 0.001). For other tissues (spleen, colon, tumor) the differences were not significant, although the whey-fed animals had the highest concentrations of glutathione (P = 0.8). Whey is a source of precursors (cysteine-rich proteins) for glutathione synthesis and may be important in providing protection to the host by stimulating glutathione synthesis. A positive correlation was observed between mean fecal fat concentrations for rats in each treatment group and large intestinal tumor burden (r² = 0.898, P = 0.05). Fecal fat could be involved in aiding initiation and/or promotion of carcinogenesis. Whatever the mechanism(s), dairy proteins, and whey proteins in particular, offer considerable protection to the host against dimethylhydrazine-induced tumors relative to the other protein sources examined.

KEY WORDS: • glutathione • fecal fat • rats • intestinal cancers • dietary proteins

¹ Supported by a research grant (no. CSt 111) from the Dairy Research and Development Corporation of Australia. Preliminary reports concerning portions of this work were presented at the World Congress of Dairy Products in Human Health and Nutrition, June 7–10, 1993, Madrid, Spain, and the American Dairy Science Association Annual Meeting, June 13–16, 1993, College Park, MD.

² The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

³ To whom correspondence and reprint requests should be addressed at CSIRO Division of Human Nutrition, P.O. Box 10041 Gouger Street, Adelaide, SA 5000, Australia.

Manuscript received 19 April 1994. Revision accepted 7 September 1994.

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