Abstract
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.
Highlights
The discovery of acrylamide, a Class 2A probable human carcinogen [1] and rodent carcinogen [2,3,4,5], in popular and fast foods [6] has raised public health concerns [7]
Acrylamide is known to cause tumors in multiple organs in rodent bioassays [1,2,4]. In these studies, the colon was not identified as a target organ for the carcinogenic effect of acrylamide
Compared to rats on a basal diet, those that were fed diets supplemented with 10% corn oil and 10% beef tallow had more, and those fed diets supplemented with 10% olive oil and 10% fish oil had fewer acrylamide-induced colon ACF [21], using a dose of acrylamide similar to that reported earlier [20]
Summary
The discovery of acrylamide, a Class 2A probable human carcinogen [1] and rodent carcinogen [2,3,4,5], in popular and fast foods [6] has raised public health concerns [7]. High levels of acrylamide are formed in foods processed at high temperatures (baking and frying) through the Maillard reaction between the amino group of asparagine and the carbonyl group of reducing sugars [8]. Foods such as French fries, potato and tortilla chips, baked foods, breakfast cereals and roasted coffee contain acrylamide at parts per million concentrations [9,10,11,12,13]. Acrylamide and its epoxide metabolite glycidamide can bind to hemoglobin and DNA to form adducts, and can interact with other proteins at the cellular level [15]. The literature is replete with experimental data supporting the risk characterization of acrylamide as a carcinogen, genotoxin and neurotoxin
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