Modification by catechol and resorcinol of upper digestive tract carcinogenesis in rats treated with methyl-N-amylnitrosamine.

Modifying effects of the environmental contaminant catechol, and its isomers resorcinol and hydroquinone, on methyl-N-amylnitrosamine (MNAN)-induced carcinogenesis were studied in male F344 rats. Groups of 15 rats were given three i.p. injections of 25 mg/kg of body weight of MNAN within the initial 2-wk period, and commencing 1 wk thereafter they were administered 0.8% catechol, 0.8% resorcinol, or 0.8% hydroquinone in powdered basal diet or were given basal diet alone for 49 wk. Additional groups of 10 to 15 rats were similarly treated without prior carcinogen exposure. Histological examination after sacrifice at wk 52 revealed that the incidences of tongue papillomas and esophageal squamous cell carcinomas in the groups given MNAN followed by catechol (57.1% and 64.3%) or resorcinol (50% and 58.8%) were significantly higher than those in the carcinogen only controls (9.1, and 0%, respectively). Hydroquinone also enhanced the development of esophageal squamous cell carcinomas but was less active than catechol or resorcinol. The incidence of alveolar hyperplasia in the lungs of the group given MNAN followed by catechol (0%) was, in contrast, significantly reduced as compared to the control value (54.5%). Hydroquinone and resorcinol showed a similar but non-significant tendency. These results indicated that the environmental contaminant, catechol and its isomers, may play a role in the development of human upper gastrointestinal cancer, in addition to exerting modifying effects in other organs.