Selenium Distribution and Human Cancer Mortality

Shamberger, Raymond J.; Willis, Charles E.

doi:10.3109/10408367109151308

Cited by 231 publications

(68 citation statements)

References 16 publications

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“…Low levels of selenium have been associated with a higher risk of cardiovascular diseases and cancer in humans, which is another important factor related to dietary intake [12] . Epidemiological studies illustrate an increased incidence of colorectal cancer in humans in geographic regions where selenium is deficient [13] . Selenium affects colon cancer susceptibility and DNA methylation.…”

Section: Introductionmentioning

confidence: 99%

Selenium as a chemopreventive agent in experimentally induced colon carcinogenesis

Ghadi

Ghara²,

Bhattacharyya³

et al. 2009

WJGO

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AIM:To elucidate the chemopreventive efficacy of selenium during experimentally induced colon carcinogenesis. METHODS:Thirty-two male wistar rats were divided into four groups: group Ⅰ (normal control); group Ⅱ [1,2-dimethylhydrazine (DMH) treated]; group Ⅲ (selenium treated); and group Ⅳ (DMH + selenium treated). Groups Ⅱ and Ⅳ were given subcutaneous injections of DMH (30 mg/kg body weight) every week for 20 wk. Selenium, in the form of sodium selenite, was given to groups Ⅲ and Ⅳ at 1 ppm in drinking water ad libitum for 20 wk. At the end of the study, rats were sacrificed and their colons were analyzed for the development of tumors, antioxidant enzyme levels and histological changes. RESULTS:100% of the DMH treated rats developed tumors, which was reduced to 60% upon simultaneous selenium supplementation. Similarly, tumor multiplicity decreased to 1.1 following selenium supplementation to DMH treated rats. Levels of lipid peroxidation, glutathione-S-transferase, superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) decreased following DMH treatment, whereas levels of glutathione (GSH) and glutathione reductase (GR) significantly increased in DMH treated rats. Selenium administration to DMH treated rats led to an increase in the levels of lipid peroxidation, SOD, catalase, glutathione-S-transferase and GPx, but decreased the levels of GSH and GR. Histopathological studies on DMH treated rats revealed dysplasia of the colonic histoarchitecture, which showed signs of improvement following selenium treatment. CONCLUSION:The study suggests the antioxidative potential of selenium is a major factor in providing protection from development of experimentally induced colon carcinogenesis.

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Section: Introductionmentioning

confidence: 99%

Selenium as a chemopreventive agent in experimentally induced colon carcinogenesis

Ghadi

Ghara²,

Bhattacharyya³

et al. 2009

WJGO

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“…Selenoproteins are enzymes that participate in oxidative defense and are thought to protect against colon cancer, especially in settings of high oxidant stress, such as chronic inflammatory states. Several epidemiological studies have inversely correlated nutritional selenium status and cancer risk, particularly in colon cancer (15). Recently, our laboratory has demonstrated that selenium deficiency in mice exacerbates intestinal injury in response to chemical models of colitis and increases tumorigenesis in CAC modeling (16).…”

Section: Introductionmentioning

confidence: 99%

Selenoprotein P influences colitis-induced tumorigenesis by mediating stemness and oxidative damage

et al. 2015

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“…It has been reported in demographic investigations that cancer mortality may be inversely related to bioavailability of selenium (27,(53)(54)(55); however, because of several problems in these studies, including difficulties in the geographical correlation of Se intakes with cancer mortality, these studies cannot be regarded as conclusive. In smelter workers exposed to arsenic and other metals, tissue selenium concentrations were lower in workers dying from malignancies (Wester, unpublished data) compared with those dying from other causes.…”

Section: Seleniummentioning

confidence: 63%