Enhancement of dopaminergic agonist bromocriptine of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats

Br J Cancer. 1992 Mar;65(3):351-4. doi: 10.1038/bjc.1992.71.

Abstract

The effects of the dopamine agonist 2-bromo-alpha-ergocryptine methanesulfonate (bromocriptine) on the incidence, number and histology of gastric cancer induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in Wistar rats. Rats were given 1 or 2 mg kg-1 body weight of bromocriptine subcutaneously every other day in depot form after 25 weeks of oral treatment with MNNG. Prolonged administration of bromocriptine at both dosages every other day resulted in a significant increase in the incidence and number of gastric cancers of the glandular stomach by week 52. Bromocriptine treatment did not influence the histological type of gastric cancer, but caused a significant increase in the labelling index of epithelial cells of the antrum. These findings indicate that the dopamine agonist bromocriptine promotes gastric carcinogenesis, and that this effect may be related to its effect in increasing proliferation of epithelial cells in the antral mucosa.

MeSH terms

  • Adenocarcinoma / chemically induced*
  • Animals
  • Bromocriptine / pharmacology*
  • Dopamine / physiology
  • Epinephrine / analysis
  • Gastric Mucosa / metabolism
  • Gastric Mucosa / physiology
  • Gastrins / blood
  • Hydrogen-Ion Concentration
  • Male
  • Methylnitronitrosoguanidine
  • Neoplasms, Experimental
  • Norepinephrine / analysis
  • Rats
  • Rats, Inbred Strains
  • Stomach Neoplasms / chemically induced*

Substances

  • Gastrins
  • Methylnitronitrosoguanidine
  • Bromocriptine
  • Dopamine
  • Norepinephrine
  • Epinephrine