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© 1994 Oxford University Press

research-article

Increased Frequency of Resistance to Terminal Differentiation in C3H Mouse Cells Produced by Genotoxic but Not Nongenotoxic Carcinogens

R. T. PRZYGODA*, J. J. FREEMAN*, S. KATZ{dagger} and R. H. MCKEE*

*Exxon Biomedical Sciences Inc. East Millstone, New Jercy 08875 {dagger}Department of Biochemistry and Microbiology Rutgers University New Brunswick, New Jersey 08903

Received September 7, 1993; accepted February 7, 1994

Certain cells present in mouse skin are resistant to calciuminduced terminal differentiation. It is believed that these calcium-resistant cells (CRCs) represent an early stage in the carcinogenic process, in part, because frequency increases after treatment with mutagens. The frequency of CRCs in C3H mouse skin was measured before and after treatment with certain petroleum-derived materials. One objective was to determine whether this assay could differentiate between genotoxic and nongenotoxic mouse skin carcinogens. An additional objective was to determine whether CRCs are an important factor in the tumorigenicity of petroleum middle distillates (PMDs), a class of apparently nongenotoxic materials. Three petroleum derived materials were tested: mineral oil (MO), a noncarcinogenic product used as the negative control; catalytically cracked clarified oil (CCCO), a highly carcinogenic and mutagenic material; and a lightly refined paraffinic oil (LRPO), a PMD which has produced tumors when repeatedly applied, but is not mutagenic and does not initiate mouse skin tumors. The CRC frequency was not increased by LRPO treatment; however, a statistically significant and dose-related increase was produced by CCCO. These results are consistent with observations that genotoxic, petroleum-derived liquids are capable of tumor initiation in mouse skin, whereas PMDs which are not genotoxic do not initiate skin tumors. The number of CRCs in untreated and MO-treated mice was approximately twice the tumor frequency measured in bioassays of PMDs. Thus, tumor production associated with these products could be due to promotion of preexisting, spontaneously initiated cells.


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