Page Banner

United States Department of Agriculture

Agricultural Research Service

Title: The Acb's (Alkylcyclobutanones) of Food Irradiation

Author
item Sommers, Christopher

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: June 2, 2004
Publication Date: August 6, 2004
Citation: Sommers, C.H. 2004. The acb's (alkylcyclobutanones) of food irradiation. ACS, August 6, 2004, Philadelphia, Pennsylvania. p.1.

Technical Abstract: Irradiation of foods for the purpose of improving microbiological safety, insect disinfestation, delay of ripening and sprouting has been an active area of research for over 45 years and has been approved by over 40 countries as a processing technology. Those approvals were made after extensive toxicological testing that included short-term genetic toxicology studies and long-term multi-generation feeding studies in animals that revealed no adverse effects, including cancer and birth defects, associated with consumption of irradiated foods. Hundreds of studies, including long-term studies in primates and short-term studies in humans have validated the safety of irradiated foods. Recently, however, it was claimed that 2-dodecylcyclobutanone (2-DCB), an alkylcylcobutanone that is found in trace quantities (ppm) in irradiated foods as a result of the radiolysis of palmitic acid, produced weak genotoxicity in a short-term DNA strand breakage test, the Comet Assay. Unfortunately, the Comet Assay has not been approved by regulatory agencies, and sometimes produces false positive results when cytotoxicity is induced. Some consumer groups have claimed results of those studies as proof that irradiated foods are both mutagenic and carcinogenic. In order to more accurately assess the genotoxicity of 2-DCB it was tested in the Escherichia coli TRP reverse and 5-fluorouracil forward mutagenicity tests, the Salmonella Mutagenicity Test, and the Yeast DEL Assay. 2-DCB did not induce mutations or chromosomal rearrangements in any of those assays, with or without exogenous metabolic activation. 2-DCB also failed to increase expression of the DNA damage inducible recA, dinD, umuDC and nfo genes in E. coli, with or without metabolic activation. The inability of 2-DCB to induce mutations, increase expression of DNA damage inducible genes, or cause genomic rearrangements in these short-term genetic toxicology tests calls into question the claims of 2-DCB's alleged genotoxic activity.

Last Modified: 8/27/2014
Footer Content Back to Top of Page