Abstract
The mouse skin carcinogenesis model provides a conceptual framework to study the carcinogenesis process. It has been used extensively to assess whether a chemical or physical agent carries a carcinogenic hazard to humans and to define the mechanism involved with the carcinogenic effects. We conducted a study to evaluate whether the tumor‐promoting activity of pentachlorophenol (PCP) is mainly from its major metabolite tetrachlorohydroquinone (TCHQ). We applied the mouse skin model to CD‐1 mice and the results showed that PCP and TCHQ are much weaker promoters than 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) in mouse skin during a 25‐wk experiment. Both PCP and TCHQ could induce mice skin epidermal hyperplasia and proliferating cell nuclear antigen (PCNA) labeling index in the epidermis. However, TCHQ caused a more significant induction of epidermal hyperplasia and PCNA positive cells than PCP. Topical application of PCP, but not TCHQ, induced significant organ enlargement and lymphoma in mice, whereas short‐term treatment of TCHQ increased tumor necrosis factor‐α (TNF‐α) gene expression in mouse skin. We did not observe a significant association between the carcinogenic process and serum TNF‐α or interleukin‐1β (IL‐1β) levels in mice. © 2003 Wiley‐Liss, Inc.