Prediagnostic Serum Selenium and Risk of Cancer

Willett, Walter C.; Morris, J. Steven; Pressel, Sara L.; Taylor, James O.; Polk, B. Frank; Stampfer, Meir J.; Rosner, Bernard; Schneider, Kenneth A.; Hames, Curtis G.

doi:10.1016/s0140-6736(83)90116-2

Cited by 492 publications

(167 citation statements)

References 36 publications

Supporting

Mentioning

150

Contrasting

Unclassified

Order By: Relevance

“…Thus, Se intake or status becomes more important when the concentration of other antioxidants or the activity of other antioxidant enzymes is low. The strongest effect of Se on cancer risk has been shown among those subjects with the lowest levels of dietary antioxidant vitamins and carotenoids (Willett et al 1983;Salonen et al 1985;Kok et al 1987;Knekt et al 1990;van den Brandt et al 1993van den Brandt et al , 2003Yu et al 1999), and particularly at low a-tocopherol concentrations (Combs & Gray, 1998). In the study of Yoshizawa et al (1998), summarised in Table 2, the inverse association between Se status and advanced prostate cancer was found to be slightly stronger after excluding men with an intake of vitamin E >30 mg/d, mostly from supplementary sources (OR 0 .…”

Section: Reduction Of Oxidative Stressmentioning

confidence: 99%

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

2005

View full text Add to dashboard Cite

Se is an unusual trace element in having its own codon in mRNA that specifies its insertion into selenoproteins as selenocysteine (SeCys), by means of a mechanism requiring a large SeCysinsertion complex. This exacting insertion machinery for selenoprotein production has implications for the Se requirements for cancer prevention. If Se may protect against cancer, an adequate intake of Se is desirable. However, the level of intake in Europe and some parts of the world is not adequate for full expression of protective selenoproteins. The evidence for Se as a cancer preventive agent includes that from geographic, animal, prospective and intervention studies. Newly-published prospective studies on oesophageal, gastric-cardia and lung cancer have reinforced previous evidence, which is particularly strong for prostate cancer. Interventions with Se have shown benefit in reducing the risk of cancer incidence and mortality in all cancers combined, and specifically in liver, prostate, colo-rectal and lung cancers. The effect seems to be strongest in those individuals with the lowest Se status. As the level of Se that appears to be required for optimal effect is higher than that previously understood to be required to maximise the activity of selenoenzymes, the question has been raised as to whether selenoproteins are involved in the anti-cancer process. However, recent evidence showing an association between Se, reduction of DNA damage and oxidative stress together with data showing an effect of selenoprotein genotype on cancer risk implies that selenoproteins are indeed implicated. The likelihood of simultaneous and consecutive effects at different cancer stages still allows an important role for anti-cancer Se metabolites such as methyl selenol formed from g-glutamyl-selenomethyl-SeCys and selenomethyl-SeCys, components identified in certain plants and Se-enriched yeast that have anti-cancer effects. There is some evidence that Se may affect not only cancer risk but also progression and metastasis. Current primary and secondary prevention trials of Se are underway in the USA, including the Selenium and Vitamin E Cancer Prevention Trial (SELECT) relating to prostate cancer, although a large European trial is still desirable given the likelihood of a stronger effect in populations of lower Se status.

show abstract

Section: Reduction Of Oxidative Stressmentioning

confidence: 99%

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

2005

View full text Add to dashboard Cite

show abstract

“…Epidemiologic studies suggest that an inverse relationship exists between serum selenium levels and cancer risk (12,13). The secondary clinical findings of Clark et al in the National Prevention of Cancer trial showed that selenium supplementation may potentially reduce the incidence of prostate cancer by 50% (14).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of androgen receptor signaling by selenite and methylseleninic acid in prostate cancer cells: two distinct mechanisms of action

Husbeck

Bhattacharyya

Feldman

et al. 2006

Molecular Cancer Therapeutics

View full text Add to dashboard Cite

The development of prostate cancer and its progression to a hormone-refractory state is highly dependent on androgen receptor (AR) expression. Recent studies have shown that the selenium-based compound methylseleninic acid (MSeA) can disrupt AR signaling in prostate cancer cells. We have found that selenite can inhibit AR expression and activity in LAPC-4 and LNCaP prostate cancer cells as well but through a different mechanism. On entering the cell, selenite consumes reduced glutathione (GSH) and generates superoxide radicals. Pretreatment with N-acetylcysteine, a GSH precursor, blocked the down-regulation of AR mRNA and protein expression by selenite and restored AR ligand binding and prostatespecific antigen expression to control levels. MSeA reacts with reduced GSH within the cell; however, Nacetylcysteine did not effect MSeA-induced downregulation of AR and prostate-specific antigen. The superoxide dismutase mimetic MnTMPyP was also found to prevent the decrease in AR expression caused by selenite but not by MSeA. A Sp1-binding site in the AR promoter is a key regulatory component for its expression. Selenite decreased Sp1 expression and activity, whereas MSeA did not. The inhibition of Sp1 by selenite was reversed in the presence of N-acetylcysteine. In conclusion, we have found that selenite and MSeA disrupt AR signaling by distinct mechanisms. The inhibition of AR expression and activity by selenite occurs via a redox mechanism involving GSH, superoxide, and Sp1.

show abstract

“…When this is not available, health can be affected, leading, in extreme cases to serious illnesses such as Keshan disease, an endemic cardiomyopathy encountered in parts of China (Institute of Medicine, 2000). Less overt Se deficiency may increase susceptibility to cardiovascular disease (Oster et al, 1986;Salonen & Huttunen, 1986;Kok et al, 1989), certain types of cancer (Willet et al, 1983;Kok et al, 1987), and possibly other disorders such as oxidative stress or inflammatory conditions, diabetes mellitus, hepatopathies, HIV infection, etc (for reviews, see Holben & Smith, 1999;Navarro-Alarcó n & Ló pez-Martínez, 2000;Rayman, 2000). In the context of these health effects, low or diminishing Se status in some parts of the world, notably in some European countries, is giving cause for concern.…”

Section: Introductionmentioning

confidence: 99%

Selenium intakes in 18–64-y-old Irish adults

et al. 2002

View full text Add to dashboard Cite

Objective: To measure the intake of selenium (Se) and the contribution of different food groups to Se intake in adults aged 18 -64 y in Ireland. The adequacy of Se intake in the population is also assessed. Design: Food consumption was estimated using a 7 day food diary for a representative sample (n ¼ 1379; men ¼ 662, women ¼ 717) of 18 -64-y-old Irish adults selected randomly from the electoral register. Se intake was estimated using updated tables of food composition. Results: Mean daily Se intakes ( AE s.d.) from all sources (ie food plus supplements), and from food sources alone, for the group of Irish adults aged 18 -64 y were 52 ( AE 23) and 50 ( AE 21) mg, respectively. Mean daily Se intake (from all sources) was significantly higher in men of all ages than women of all ages at levels of 60 and 44 mg, respectively (P < 0.001). Meat=meat products (30%), bread and rolls (24%), fish=fish products ( $ 11%), and milk and yoghurt (9%) were the main contributors to mean daily Se intake. Adequacy of Se intake in population groups was estimated as the percentage of the population with mean daily Se intakes that were lower than the average requirement of 40 mg. Using this measure, 45.6% of women and 17.1% of men had inadequate Se intakes.

show abstract

Prediagnostic Serum Selenium and Risk of Cancer

Cited by 492 publications

References 36 publications

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

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

Inhibition of androgen receptor signaling by selenite and methylseleninic acid in prostate cancer cells: two distinct mechanisms of action

Selenium intakes in 18–64-y-old Irish adults

Contact Info

Product

Resources

About