[Effect of vitamin E and selenium deficiency on esophageal tumorigenesis and its oxidative stress mechanism]

To explore the effect of vitamin E (VE) and selenium (Se) deficiency on esophageal tumorigenesis and its oxidative stress mechanism.

110 male F344 rats were randomly divided into 3 groups: VE/Se deficient group (group A), VE/Se normal group (group B) and control group (group C). Animals in group A and group B were subcutaneously injected with N-nitrosomethylbenzylamine (NMBzA) at the dosage of 0.35 mg/kg BW, 3 times per week for 5 weeks. Control group was given the solvent 20% DMSO as negative control. Animals in group A were fed with low-VE/Se diet (46IU/kg VE, 0.05 mg/kg Se), animals in group B and C were fed with normal diet (80IU/kg VE, 0.15 mg/kg Se). Animals were sacrificed to perform macroscopic observation and pathologic inspection at the 25th week of the experiment. Plasma VE level was determined by high-performance liquid chromatography, and Se level was determined by fluorescence method. Cell proliferation and DNA damage in esophagus were detected through immunohistochemistry of BrdU and 8-OH-dG, respectively. Glutathione peroxidase (GPX) and glutathione transferase (GST) activities in plasma, esophagus and liver were analyzed by using test kits.

VE/Se levels of group A were significantly lower than those of group B, the later were slightly lower than those of group C. Visible tumor incidence, tumor multiplicity and pathologic lesions in group A were all significantly more than those in group B. Comparing with group B, cell proliferation and 8-OH-dG levels were also significantly increased in group A. GPX and GST activities in plasma, esophagus and liver of group A were significantly higher than those of group B.

Vitamin E and selenium deficiency significantly promoted the NMBzA-induced esophageal tumorigenesis. Oxidative stress and DNA damage may be one of the critical routes by which NMBzA induces carcinogenesis in rat esophagus.