Genotoxic properties of 2-dodecylcyclobutanone, a compound formed on irradiation of food containing fat

When food containing fat is treated by ionizing radiation, a group of 2-alkylcyclobutanones is formed. These components contain the same number of carbon atoms as their precursor fatty acids and the alkyl group is located in ring position 2. Thus, from palmitic acid 2-dodecylcyclobutanone is derived. To date, there is no evidence that the cyclobutanones occur in unirradiated food. Therefore, these components cannot be considered inherent to food, and for questions pertaining to risk assessment of irradiated food it would be advisable to determine the genotoxic and toxic potentials of cyclobutanones. Measurements of DNA damage in cells exposed to 2-dodecylcyclobutanone, employing the single cell microgel electrophoresis technique, have been carried out. In vitro experiments using rat and human colon cells indicate that 2-docylcyclobutanone in the concentration range of about 0.30 – 1.25 mg/ml induces DNA strand breaks in the cells. Simultaneously, a concentration related cytotoxic effect is observed as was determined by trypan blue exclusion. To which extent these in vitro findings are of relevancy for the in vivo human exposure situation needs to be investigated in further studies. In vivo tests in rats are in progress.     

Colon cancer risk factors from nutrition

Nutrition and health are closely connected and malnutrition can seriously endanger health. The consequences are higher risks of developing diseases. Of these, cancers are of special importance. The most frequent nutrition-associated type of cancer is colon cancer. This review summarises the predisposing factors for the development of colon cancer, and molecular mechanisms responsible for sporadic colon cancer. Moreover, it is pointed out that individual genetic predisposition such as polymorphisms of biotransformation systems might affect susceptibility to cancer risk factors. Selected findings of epidemiological research and nutritional habits, foods, and metabolites that could increase cancer risk are discussed. Furthermore, toxicological assessment of food-related risk factors, e.g. heterocyclic amines, and potential protective effects of food ingredients, e.g. the induction of phase II enzymes or removal of already degenerated cells from tissue by apoptosis, inhibition of proliferation, and cell differentiation are discussed. Risks are not necessarily reduced by avoiding certain substances but by healthy and well-balanced nutrition. Knowledge of individual susceptibility will also make it possible to recognise risks and design more specific nutritional recommendations.