Acrylamide, a possible human
carcinogen, is formed in certain
carbohydrate-rich foods processed at high temperature. We evaluated if dietary acrylamide, at doses (0.5, 1.0 or 2.0 mg/kg diet) reflecting upper levels found in human foods, modulated colon
tumorigenesis in two rodent models. Male F344 rats were randomized to receive diets without (control) or with acrylamide. 2-weeks later, rats in each group received two weekly
subcutaneous injections of either
azoxymethane (AOM) or saline, and were killed 20 weeks post-
injections; colons were assessed for
tumors. Male athymic nude (nu/nu) mice bearing HT-29 human
colon adenocarcinoma cells-derived
tumor xenografts received diets without (control) or with acrylamide;
tumor growth was monitored and mice were killed 4 weeks later. In the F344 rat study, no
tumors were found in the colons of the saline-injected rats. However, the colon
tumor incidence was 54.2% and 66.7% in the control and the 2 mg/kg acrylamide-treated AOM-injected groups, respectively. While
tumor multiplicity was similar across all diet groups,
tumor size and burden were higher in the 2 mg/kg acrylamide group compared to the AOM control. These results suggest that acrylamide by itself is not a "complete
carcinogen", but acts as a "co-
carcinogen" by exacerbating the effects of AOM. The nude mouse study indicated no differences in the growth of human colon
tumor xenografts between acrylamide-treated and control mice, suggesting that acrylamide does not aid in the progression of established
tumors. Hence, food-borne acrylamide at levels comparable to those found in human foods is neither an independent
carcinogen nor a
tumor promoter in the colon. However, our results characterize a potential hazard of acrylamide as a colon co-
carcinogen in association with known and possibly other environmental
tumor initiators/promoters.