Selenium

About: Selenium is a research topic. Over the lifetime, 21192 publications have been published within this topic receiving 429715 citations. The topic is also known as: Se & selen.

Selenium Inhibition of N-Methyl-N-nitrosourea-Induced Mammary Carcinogenesis in the Rat, ,

Abstract: The effect of supplemental dietary selenium on the postinitiation state of N-methyl-N-nitrosourea (MNU)-induced mammary carcinogenesis was investigated in noninbred female Sprague-Dawley rats. Mammary cancer was induced by a single iv injection of MNU. Supplemental selenium feeding was begun 7 days after carcinogen treatment. Feeding of selenium prolonged the latency of mammary cancer appearance and resulted in a reduction in the average number of cancers per rat. The results suggested an inhibitory effect of pharmacologic levels of dietary selenium on the postinitiation stage of mammary carcinogenesis.

Glutathione peroxidase activity as a function of dietary selenomethionine

Abstract: SINCE 1957, selenium has been recognized as an essential micronutrient for animals, but its exact biological function has remained uncertain. The metabolic role of selenium in animals seems to be linked with vitamin E and sulphur amino acids1–4. Selenium has a sparing effect on vitamin E, and delays the onset of deficiency syndromes. Likewise, vitamin E and sulphur amino acids partially protect against or delay the onset of several forms of selenium deficiency syndromes. Rotruck et al.5 proposed that selenium functions as an integral part of glutathione (GSH) peroxidase, an enzyme that reduces toxic lipid peroxides to hydroxy acids6–8. They found that a large proportion of the 75Se from rat erythrocytes labelled in vivo remained with the enzyme during extensive purification, and more recently, their studies with highly purified GSH peroxidase have indicated that it contains approximately 4 mol of Se per mol of enzyme9. Similar findings were reported by Flohe et al. for bovine erythrocyte GSH peroxidase10. To learn more about the nutritional relationship between selenium and GSH peroxidase, we performed studies that showed GSH peroxidase activity is proportional to dietary selenium, which provided additional evidence for the role of selenium in the function of GSH peroxidase.

Association between serum selenium level and type 2 diabetes mellitus: a non-linear dose-response meta-analysis of observational studies

Abstract: The association between serum selenium levels and type 2 diabetes mellitus (T2DM) is controversial. We performed a systematic review and non-linear dose–response meta-analysis of observational studies to investigate the association in the present study. A comprehensive literature search was conducted using MEDLINE and EMBASE databases. A pooled odds ratio (OR) and related 95 % confidence interval (95 % CI) for T2DM between the highest and lowest serum selenium categories, and a non-linear dose–response relationship between selenium and T2DM were estimated. A total of five studies (of 13,460 participants) were identified as meeting the inclusion criteria. The pooled OR indicated that there was a significantly higher prevalence of T2DM in the highest category of blood selenium compared with the lowest (OR = 1.63, 95 % CI: 1.04–2.56, P = 0.033). Moreover, a significant non-linear dose–response relationship was observed between serum selenium levels and T2DM (P 132.5 μg/l). The positive association between serum selenium levels and T2DM existed in populations with relatively low levels and high levels of serum selenium, indicating a likely U-shaped non-linear dose–response relationship between serum selenium and T2DM.

Dietary Selenite and Azadeoxycytidine Treatments Affect Dimethylhydrazine-Induced Aberrant Crypt Formation in Rat Colon and DNA Methylation in HT-29 Cells

Abstract: Several observations implicate a role for altered DNA methylation in cancer pathogenesis. The global level of DNA methylation is generally lower; however, DNA methyltransferase (Dnmt1) activity is usually higher in tumor cells than in normal cells. The purpose of this study was to investigate whether the Dnmt1 inhibitor, 5-aza-2'-deoxycytidine (aza-dC) would alter the effect of dietary selenium on the formation of aberrant crypts. Weanling rats (n = 60) were fed three concentrations of selenium (deficient, 0.1 and 2.0 mg/kg diet) in a Torula yeast-based diet. Half of the rats were injected weekly with aza-dC (1 mg/kg, subcutaneously) and half were injected with the vehicle control (PBS). After 3.5 wk of consuming the experimental diets, the rats were given two injections of dimethylhydrazine (DMH; 25 mg/kg, intraperitoneally). Rats fed the selenium-deficient diet and injected with PBS had significantly (P < 0.006) more aberrant crypts than rats fed 0.1 or 2.0 mg selenium/kg diet (244 +/- 21 vs. 165 +/- 9 and 132 +/- 14, respectively). In contrast, when rats were injected with aza-dC, there was a significant (P < 0.0001) reduction in aberrant crypt formation and dietary selenium had no effect (62 +/- 8 vs. 77 +/- 13 vs. 54 +/- 8, in rats fed 0, 0.1 and 2.0 mg selenium/kg diet, respectively). HT-29 cells cultured in the absence of selenium had significantly hypomethylated DNA but significantly more Dnmt1 protein expression than cells cultured in the presence of 1 or 2 micromol/L selenium. These results suggest that aza-dC treatment may protect selenium-deficient rats against carcinogen-induced aberrant crypt formation.