AIM: To investigate the effect and significance of selenium in early experimental gastric carcinogenesis. METHODS: Weaning male Wistar rats were divided randomly into normal control group, experiment control group, low selenium (2 mg/L) group and high selenium (4 mg/L) group. Wistar rat gastric carcinogenesis was induced by /V-methyl-/V-nitro-/V-nitroso guanidine (MNNG) (20 mg/kg) gavage daily for 10 d. Na_2SeO_3 was given by piped drinking 1 wk prior to MNNG gavage. The rats were killed at the 43~(rd) wk. The surface characteristics of gastric mucosa were observed with naked eyes. Histopathologic changes of rat gastric mucosa were observed by HE staining and AB-PAS methods. The changes of cellular ultrastructure were observed under transmission electron microscope. Statistical analysis was carried out by SPSS. RESULTS: The incidence rate of gastric mucosa erosion, hemorrhage and intestinal metaplasia was 0, 45.5%, 66.7%, and 92.9%, respectively (92.9% vs 45.5%, P<0.05) in the normal control group, experiment control group, low selenium group, and high selenium group. Leiomyoma formed in the process of inducement of rat gastric carcinoma. Dietary Na_2SeO_3 (2 and 4 mg/L) slightly increased the incidence rate of leiomyoma (0, 23%, 46.6%, and 46.6%). gastric mucosa did not change in the course of rat gastric carcinogenesis. Dietary Na_2SeO_3 by pipe drinking could expand the intracellular secretory canaliculus of parietal cells and increase the number of endocrine cells and lysosomes. CONCLUSION: Dietary Na_2SeO_3 by pipe drinking aggravates gastric erosion, hemorrhage and promotes intestinal metaplasia of gastric mucosa. The mechanism may be related with the function of parietal cells. AIM: To investigate the effect and significance of selenium in early experimental gastric carcinogenesis. METHODS: Weaning male Wistar rats were divided randomly into normal control group, experiment control group, low selenium (2 mg / L) group and high selenium (4 mg / L) group. Wistar rat gastric carcinogenesis was induced by / V-methyl- / V-nitro- / V- nitroso guanidine (MNNG) (20 mg / kg) gavage daily for 10 d. Na_2SeO_3 was given by piped drinking 1 wk prior The rats were killed at the 43 ~ (rd) wk. The surface characteristics of gastric mucosa were observed with naked eyes. Histopathologic changes of rat gastric mucosa were observed by HE staining and AB-PAS methods. The changes of cellular RESULTS: The incidence rate of gastric mucosa erosion, hemorrhage and intestinal metaplasia was 0, 45.5%, 66.7%, and 92.9% respectively (92.9% vs 45.5%, respectively) , P <0.05) in the normal c ontrol group, experiment control group, low selenium group, and high selenium group. Leiomyoma formed in the process of inducement of rat gastric carcinoma. Dietary Na_2SeO_3 (2 and 4 mg / L) , 46.6%, and 46.6%). Gastric mucosa did not change in the course of rat gastric carcinogenesis. Dietary Na_2SeO_3 by pipe drinking could expand the intracellular secretory canaliculus of parietal cells and increase the number of endocrine cells and lysosomes. CONCLUSION: Dietary Na_2SeO_3 by pipe drinking aggravates gastric erosion, hemorrhage and promotes intestinal metaplasia of gastric mucosa. The mechanism may be related with the function of parietal cells.