Journal Article

Effects of vitamin E and selenium supplementation on esophageal adenocarcinogenesis in a surgical model with rats

Xiaoxin Chen, Samer S. Mikhail, Yu Wei Ding, Guang-yu Yang, Floredeliza Bondoc and Chung S. Yang

in Carcinogenesis

Volume 21, issue 8, pages 1531-1536
Published in print August 2000 | ISSN: 0143-3334
Published online August 2000 | e-ISSN: 1460-2180 | DOI:
Effects of vitamin E and selenium supplementation on esophageal adenocarcinogenesis in a surgical model with rats

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Two well-known antioxidative nutrients, vitamin E and selenium, were used in this study to investigate possible inhibitory action against the formation of esophageal adenocarcinoma (EAC) in rats. In this model, carcinogenesis is believed to be driven by oxidative stress. Male Sprague–Dawley rats (8 weeks old) were divided into four groups and received esophagoduodenal anastomosis (EDA) surgery plus iron supplementation (12 mg/kg/week). Vitamin E and selenium were supplemented in the diet in the forms of α-tocopheryl acetate (750 IU/kg) and sodium selenate (1.7 mg Se/kg), which were 10 times the regular amounts in the basic AIN93M diet. At 40 weeks after surgery, all the EDA groups had lower body weights than the non-operated control group. Iron nutrition (hemoglobin, total serum iron and transferrin saturation) was normal as a result of iron supplementation after EDA. Vitamin E supplementation maintained the normal plasma level of α-tocopherol in EDA rats, but not those of γ-tocopherol and retinol. Selenium supplementation increased the serum and liver selenium contents of the EDA rats. Histopathological analysis showed that selenium supplementation increased the incidence of EAC and the tumor volume. The selenium level in the tumor is higher than that in the duodenum of the same animal.Vitamin E supplementation, however, inhibited carcinogenesis, especially in the selenium-supplemented group. We believe that vitamin E exerts its effect through its antioxidative properties, and a high dose of inorganic selenium may promote carcinogenesis by enhancing oxidative stress.

Keywords: CLE, columnar-lined esophagus; EAC, esophageal adenocarcinoma(s); EDA, esophagoduodenal anastomosis; ICP ES/MS, inductively coupled plasma emission spectrometry/mass spectrometry; ROS, reactive oxygen species.

Journal Article.  5334 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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