Induction of beta-glucuronidase activity during dimethylhydrazine carcinogenesis and additive effects of cholic acid and indole.

Abstract

The kinetic change of beta-glucuronidase (beta-G) activity was measured in mouse large intestinal mucosa during dimethylhydrazine (DMH) carcinogenesis with addition of cholic acid and/or indole. The experiment lasted 21 weeks. The enzyme activity began to increase significantly at 5th week after treatment of DMH with cholic acid and/or indole, and at 7th week with DMH alone. Then, increased activity remained the rest of the time. Mouse intestinal cancer induced by DMH injection are also shown to have an increased beta-G activity. The induction of beta-G activity in the early stage of DMH colon carcinogenesis and additive effects of cholic acid and/or indole may imply one mechanism of action of DMH as a carcinogen and cholic acid as a promoter in large intestinal cancer.

• Authors: Y Sun, Y Li
• Journal: Cancer letters (Cancer Lett) Vol. 39 Issue 1 Pg. 69-76 (Feb 1988) ISSN: 0304-3835 [Print] Ireland
• PMID: 3345507 (Publication Type: Journal Article)

Chemical References

• Cholic Acids
• Dimethylhydrazines
• Indoles
• Methylhydrazines
• Glucuronidase

Topics

• Adenocarcinoma (chemically induced, enzymology)
• Animals
• Cholic Acids (pharmacology)
• Cocarcinogenesis
• Colonic Neoplasms (chemically induced, enzymology)
• Dimethylhydrazines (toxicity)
• Enzyme Activation (drug effects)
• Female
• Glucuronidase (metabolism)
• Hyperplasia (pathology)
• Indoles (pharmacology)
• Intestinal Mucosa (enzymology)
• Intestine, Large (enzymology, pathology)
• Methylhydrazines (toxicity)
• Mice