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Inhibition by Dietary Selenium of Colon Cancer Induced in the Rat by Bis(2-oxopropyl)nitrosamine¹

Eppley Institute for Research in Cancer, University of Nebraska Medical Center, Omaha, Nebraska 68105

Wistar-derived MRC rats were fed casein diets supplemented with 0.1 or 2.0 ppm selenium as sodium selenite from 7 weeks of age. At 8 weeks, weekly injections (5 mg/kg body weight s.c.) of bis(2-oxopropyl)nitrosamine (BOP) were started. Rats were killed after 50 injections; blood samples were collected after 1, 10, 25, and 50 weeks; and tissue samples were retained at killing for measuring hematology and selenium status. Carcinogen treatment did not influence body weight or survival. The high selenium level reduced female growth and improved male survival. Hemoglobin was reduced and mean corpuscular volume was increased in both sexes by feeding high-selenium diets. In addition, white blood cell counts were increased in BOP-treated males. Blood, liver, pancreas, and kidney selenium rose in rats fed the high-selenium diets. BOP treatment reduced liver selenium at the low dietary level and increased pancreas selenium at the high level. Glutathione peroxidase values in erythrocytes and plasma increased with the high-selenium diets, whereas its activity in the liver was not influenced by dietary selenium but was reduced in male rats by BOP treatment. Colon adenocarcinoma yield was reduced in male rats fed the high selenium level (16 carcinomas in 30 rats) by comparison with the low selenium level (28 carcinomas in 29 rats). Lung adenocarcinoma incidence decreased to none in 30 male rats fed the high-selenium diet from 4 in 29 male rats (14%) given the low selenium level. Female rats did not develop colon or lung adenocarcinomas at either selenium level. The influence of dietary selenium in the colon was related to an increased repair rate of BOP-induced DNA damage in this tissue.

¹ Supported by USPHS Grant R01 CA 24549 from the National Cancer Institute.

Received 4/19/82. Accepted 8/ 4/82.

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