Submitted to: Journal of Food Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/22/2006
Publication Date: N/A
Citation: N/A Interpretive Summary: Ionizing radiation inactivates pathogenic bacteria such as E. coli O157:H7, L. monocytogenes, and Salmonella in meat and poultry, and irradiation of meat and poultry are an FDA approved process that can be used to protect consumers. The chemical changes in foods caused by irradiation are almost identical to those caused by cooking, with the exception of a chemical called 2-dodecylcyclobutanone (2-DCB), which is formed from palmitic acid, the most abundant fatty acid in the human diet. Research has shown that high fat diets increase the risk of colon cancer in rodents and humans and palmitic acid may cause breakage of chromosomes in rodent and human cells. We wanted to determine if 2-DCB could be a problem similar to palmitic acid. Using a well-established test, the micronucleus assay, to detect the breakage of chromosomes, we found that 2-DCB could only weakly increase the frequency of chromosome breakage in human cells. Because there is over one million times the amount of palmitic acid in irradiated meat than 2-DCB, it is highly unlikely that 2-DCB poses a risk to human health. These results are in agreement with previous studies in animals, conducted over the last fifty years, which have found no increased risk of cancer or birth defects from consumption of irradiated foods. Consumers will benefit from factual and accurate information pertaining to the toxicological safety of irradiated foods.
Technical Abstract: Palmitic acid, the most abundant fatty acid in the human diet, causes oxidative DNA damage, DNA strand breakage, necrosis and apoptosis in human and rodent cells in vitro, while excess fatty acids in the diet increase the risk of colon cancer in vivo. Irradiation of palmitic acid leads to the formation of 2-dodecylcyclobutanone (2-DCB), a unique radiolytic product formed at part-per-million levels in fats. Recent research has raised the possibility that, like palmitic acid, 2-DCB can also cause DNA strand breaks in human and rodent cells. In order to more fully understand the clastogenic potential of 2-DCB it was tested for the ability to induce the formation of micronuclei (MN) in human TK6 lymphoblasts. TK6 lymphoblasts were exposed to 13.3, 26.5 and 53uM of 2-DCB for 24 hrs, both with and without exogenous metabolic activation (EMA). The number of MN per binucleated cells was induced 2.65 fold without EMA, and 2.85 fold in the presence of EMA at the highest 2-DCB concentration of 53 uM. Cytotoxicity of the TK6 lymphoblasts treated with 53 uM 2-DCB was 51.7 percent in the absence of EMA, and 61.7 percent in the presence of EMA. Thus, like palmitic acid, 2-DCB may be weakly clastogenic against human cells in vitro, and given the amount of 2-DCB that would be consumed versus that of its parent fatty acid, is unlikely to have any significant impact on human health.