Genetic Toxicology Testing

During the 1970s an intensive research effort was devoted to the development of techniques to investigate chemical-induced genetic damage in a variety of cells and organisms. The impetus for this research was provided, in the first place, by the realization that chemicals were capable of producing mutations in mammalian cells that may eventually increase the incidence of heritable disease in man and, secondly, the desire to find quick and inexpensive assays to detect chemicals with carcinogenic potential. Mutations are usually the result of an interaction of the chemicals with DNA, and it was generally accepted that the cellular changes associated with chemical-induced neoplasia were also responses to an interaction with DNA. It is now evident that, although the initial stages of neoplastic transformation probably require a change in DNA structure caused by a mutagenic carcinogen, other carcinogens do not react directly with DNA and exert their effects on other stages of the carcinogenic process, e.g. carcinogen enhancers[1]. Thus most of the current short-term assays for mutagenic and carcinogenic chemicals are based on interaction with DNA resulting in gene mutations, chromosomal aberrations, unscheduled DNA synthesis, etc.