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Enhancement by Methionine Enkephalin of Colon Carcinogenesis Induced by Azoxymethane

Departments of Gastrointestinal Oncology [H. I., M. T., M. B.], Gastroenterology [S. O.], and Pathology [H. T.], The Center for Adult Diseases, Osaka 3-3, Nakamichi 1-chome, Higashinari-ku, Osaka 537, Japan

The effect of the opioid receptor agonist methionine enkephalin (Metenkephalin) and the opioid receptor antagonist naloxone on colonic carcinogenesis induced by azoxymethane was investigated in Wistar rats. Rats received ten weekly injections of 7.4 mg/kg of body weight of azoxymethane and injections of Met-enkephalin (50 µg/kg of body weight), naloxone (2 mg/kg of body weight), or Met-enkephalin (50 µg/kg of body weight) plus naloxone (2 mg/kg of body weight) once every 2 days. In wk 40, the group treated with Met-enkephalin had a significantly increased incidence of colonic tumors. A combination of Met-enkephalin and naloxone attenuated the enhancing effect by Met-enkephalin on the development of colonic tumors. Administration of naloxone alone had no influence on colonic tumorigenesis. During and after administration of the carcinogen, the bromodeoxyuridine-labeling indices of the colon mucosa and/or cancers were significantly increased in rats treated with Met-enkephalin. However, a combination of Met-enkephalin and naloxone significantly decreased the labeling indices of the colon mucosa and/or cancers. These findings indicate that Met-enkephalin enhanced colon carcinogenesis and that naloxone attenuated this enhancement. Because naloxone is an opioid receptor antagonist, these findings also indicate that the enhancing effect of Met-enkephalin on colon carcinogenesis may be mediated through opioid receptors.

¹ To whom requests for reprints should be addressed.

Received 8/ 1/90. Accepted 11/ 9/90.