The sustained development of preneoplastic lesions depends on high protein intake

Abstract

The effects of sequential alterations in the feeding of two levels of dietary protein (5% and 20% casein) on the postinitiation development of aflatoxin B1- (AFB1) induced gamma-glutamyl transpeptidase-positive (GGT+) preneoplastic foci were examined. Weanling male Fischer 344 rats fed AIN-76A diet (20% protein) were administered 10 intragastric doses of AFB1 (1 dose/day during the 14-day dosing period excluding weekends) at 250 micrograms/kg body wt (initiation). After AFB1 tissue clearance, rats were randomly assigned to dietary treatment groups. During the next 12 weeks (promotion), they developed AFB1-induced GGT+ preneoplastic lesions. The 12-week promotion period was subdivided into four three-week periods, during which rats were fed isocaloric diets containing 20% casein during all four periods (20:20:20:20), 5% casein during all four periods (5:5:5:5), or sequentially altered casein levels (20:5:20:5 and 5:20:5:20). Rats were killed at 3,6,9, and 12 weeks to examine the dependence of GGT+ foci development on protein intake. Animals fed 5% casein diets developed significantly fewer (p < 0.01) GGT+ foci than animals fed 20% casein diets despite greater total caloric intake. Similarly, in the intervention groups, preneoplastic development was enhanced when the 20% casein diet was fed and inhibited when the 5% casein diet was fed. These results indicate that the sustained development of AFB1-induced preneoplastic foci depends on a high protein intake. Alternatively, these results suggest that low protein intake inhibits lesion development.

Oxidative DNA damage induced by homogentisic acid, a tyrosine metabolite

“…Significantly increased risks of renal cell cancer were observed with increasing consumption of high protein foods [5]. An animal experiment has demonstrated that high protein intake enhanced the development of chemically induced preneoplastic foci [6]. However, the mechanism of carcinogenesis caused by protein intake remains to be clarified.…”

Renal Carcinogenicity of Concurrently Administered Fish Meal and Sodium Nitrite in F344 Rats

“…Epidemiological studies have suggested, for example, a link with cancer of the colon and rectum 10) in particular, as well as the breast 11) and kidney. 12) Experimental studies have also provided evidence that high protein intake enhances carcinogen-induced proliferative lesion development in diverse tissues including the liver 13) and colon. 14) For example, with aflatoxin B 1induced rat hepatocarcinogenesis, treatment with a high protein (20% casein) diet significantly increased the development of preneoplastic γ-glutamyltranspeptidase-positive foci as compared with the low protein (5% casein) case.…”

Meat and cancer: meat as a component of a healthy diet

“…Proteins and the insulin resistance hypothesis It has been assumed, based on per capita protein intake and colon cancer risk, that total protein is related to colon cancer risk (Youngman & Cambell, 1998). However the majority of epidemiological cohort and case -control studies could not confirm these assumptions.…”