Selenium in cancer prevention: a review of the evidence and mechanism of action

Rayman, Margaret P.

doi:10.1079/pns2005467

Cited by 754 publications

(550 citation statements)

References 113 publications

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“…Therefore, the consequence of an up-regulation of Nrf2 target genes for colorectal cancer in selenium-deficiency can not be easily defined. The activation of the Wnt pathway in seleniumdeficiency points to a cancer-promoting function of a lowselenium status and is in accordance with the higher cancer incidence in selenium-deficiency (reviewed in [46]). Whether the activation of the Nrf2 pathway is the attempt to compensate for the loss of selenoproteins with the strengthening of the endogenous defense system or whether it already contributes to survival of cancer cells is a challenge for further investigations.…”

Section: Discussionmentioning

confidence: 67%

Nrf2 target genes are induced under marginal selenium-deficiency

et al. 2010

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A suboptimal selenium supply appears to prevail in Europe. The current study, therefore, was focused on the changes in gene expression under a suboptimal selenium intake. Previous microarray analyses in the colon of mice fed either a selenium-adequate or a moderately deficient diet revealed a change in genes of several pathways. Severe selenium-deficiency has been found previously to influence Nrf2-regulated genes of the adaptive response. Since the previous pathway analyses were done with a program not searching for Nrf2 target genes, respective genes were manually selected and confirmed by qPCR. qPCR revealed an induction of phase II (Nqo1, Gsts, Sult1b1 and Ugt1a6) and antioxidant enzymes (Hmox1, Mt2, Prdx1, Srxn1, Sod1 and Gclc) under the selenium-poor diet, which is considered to compensate for the loss of selenoproteins. The strongest effects were observed in the duodenum where preferentially genes for antioxidant enzymes were up-regulated. These also include the mRNA of the selenoproteins TrxR1 and GPx2 that would enable their immediate translation upon selenium refeeding. The down-regulation of Gsk3b in moderate selenium-deficiency observed in the previous paper provides a possible explanation for the activation of the Nrf2 pathway, because inhibition of GSK3b results in the nuclear accumulation of Nrf2.

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Section: Discussionmentioning

confidence: 67%

Nrf2 target genes are induced under marginal selenium-deficiency

et al. 2010

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“…The geochemistry of Se described earlier provides a guide to the relative amounts of Se that may be expected in a particular geological setting and studies of Se in the soil, drainage sediments, water and crops give an indication of environmental Se status. It has been noted that there is a marked variation in Se intake and status (as measured in blood, plasma or serum, toenails or hair) from one part of the world to another and even between different parts of the same country (41,45) . Fig.…”

Section: Selenium Status In Human Subjects Is Linked To the Environmentmentioning

confidence: 99%

Symposium on ‘Geographical and geological influences on nutrition’ Factors controlling the distribution of selenium in the environment and their impact on health and nutrition

2009

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Se is essential to human and animal health but can be toxic in excess. An interest in its geochemistry has developed alongside a greater understanding of its function in a number of health conditions. Geology exerts a strong control on the Se status of the surface environment; low-Se rock-types (0·05–0·09 mg Se/kg) make up the majority of rocks occurring at the Earth's surface, which in turn account for the generally low levels of Se in most soils. However, there are exceptions such as associations with sulfide mineralisation and in some types of sedimentary rocks (e.g. black shales) in which contents of Se can be much higher. Baseline geochemical data now enable a comparison to be made between environmental and human Se status, although a direct link is only likely to be seen if the population is dependent on the local environment for sustenance. This situation is demonstrated with an example from the work of the British Geological Survey in the Se-deficiency belt of China. The recent fall in the daily dietary Se intake in the UK is discussed in the context of human Se status and declining use of North American wheat in bread making. Generally, US wheat has ten times more Se than UK wheat, attributed to the fact that soils from the wheat-growing belt of America are more enriched in Se to a similar order of magnitude. In agriculture effective biofortification of crops with Se-rich fertilisers must be demonstrably safe to the environment and monitored appropriately and baseline geochemical data will enable this process to be done with confidence.

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“…We hypothesized that the promoting activities of PCBs would be inhibited, since selenium is a component of the antioxidant enzymes glutathione peroxidase and thioredoxin reductase (Rayman 2005;Tapiero et al 2003). An AIN-93 torula-based purified diet containing 0.02 (deficient), 0.2 (adequate), or 2.0 mg (supplemental) selenium/kg diet was fed to SpragueDawley female rats starting ten days after administering a single dose of DEN (150 mg/kg).…”

Section: Seleniummentioning

confidence: 99%

Role of oxidative stress in the promoting activities of PCBs

Glauert

Tharappel

et al. 2008

Environmental Toxicology and Pharmacology

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PCBs are organic pollutants that persist and bioaccumulate in the environment. These chemicals induce and promote liver tumors in rodents. Previous studies have shown that they increase oxidative stress in the liver, including lipid peroxidation, oxidative DNA damage, and NF-κB activation. The objective of these studies was to determine if the promoting activities of PCBs could be inhibited by dietary antioxidants (vitamin E, selenium, or phytochemicals) or by knocking out the p50 subunit of NF-κB. In the antioxidant studies, female rats were first injected with DEN (150 mg/kg) and then administered 4 biweekly i.p. injections (300 μmol/kg/injection) of PCB-77, PCB-153, or vehicle; the number and volume of placental glutathione S-transferase (PGST)-positive foci were then quantified. Vitamin E did not influence the promoting activities of PCBs. Increasing dietary selenium above the recommended intake increased the number of foci induced but decreased their volume. Most of the phytochemicals examined (N-acetyl cysteine, β-carotene, resveratrol, EGCG) had no significant effect on the promoting activity of PCB-77. Ellagic acid increased and lycopene decreased the number of foci; ellagic acid, CoQ 10 , and curcumin decreased the volume of foci. In the NF-κB knockout study, male mice were first injected with DEN (90 mg/kg); controls not receiving DEN were also studied. Both p50 −/− and wild-type mice were then injected biweekly 20 times with PCB-153 (300 (μmol/kg). In DEN-treated and DEN + PCB-treated mice, the incidence of tumors was lower in the p50 −/− mice than in wild-type mice. In mice receiving PCB-153, the tumor incidence and tumor volume were higher. The volume of tumors that were positive for glutamine synthetase was increased in mice administered PCB-153. This study shows that the promotion of hepatocarcinogenesis by PCBs is largely unaffected by dietary antioxidants but is diminished when NF-κB activation is impaired by the absence of the p50 subunit.

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Selenium in cancer prevention: a review of the evidence and mechanism of action

Cited by 754 publications

References 113 publications

Nrf2 target genes are induced under marginal selenium-deficiency

Nrf2 target genes are induced under marginal selenium-deficiency

Symposium on ‘Geographical and geological influences on nutrition’ Factors controlling the distribution of selenium in the environment and their impact on health and nutrition

Role of oxidative stress in the promoting activities of PCBs

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