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Inhibition by -Amino-n-butyric Acid and Baclofen of Gastric Carcinogenesis Induced by N-Methyl-N'-nitro-N-nitrosoguanidine in Wistar Rats

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

The effect of -amino-n-butyric acid (GABA), the GABA_A receptor agonist muscimol (5-aminomethyl-3-hydroxyisoxazole), and the GABA_B receptor agonist baclofen [4-amino-3-(4-chlorophenyl)butanoic acid] on the incidence and number of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine was investigated in Wistar rats. Rats received alternate-day i.p. injections of 500 or 1000 mg/kg of body weight GABA, 0.25 or 0.5 mg/kg of body weight muscimol, or 4 or 8 mg/kg of body weight baclofen after 25 wk of p.o. treatment with the carcinogen. Prolonged administration of GABA at 1000 mg/kg of body weight, but not at 500 mg/kg of body weight, and of baclofen at 4 and 8 mg/kg of body weight significantly decreased the incidence and number of gastric cancers of the glandular stomach in Wk 52, but long-term muscimol administration had no influence. Histologically, GABA at the high dosage and baclofen at both dosages significantly decreased the labeling index of the antral mucosa and significantly increased the serum gastrin level. Furthermore, baclofen at both dosages significantly decreased antral pH and significantly increased gastric acid secretion. These findings indicate that GABA inhibits gastric carcinogenesis via the GABA_B receptor and that this effect may be related to its effect in decreasing the proliferation of antral mucosa.

¹ To whom requests for reprints should be addressed.

Received 9/14/89. Revised 2/26/90.

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