Four selenoproteins, protein biosynthesis, and Wnt signalling are particularly sensitive to selenium intake in mice colon

A. Kipp, A. Banning, E.M. van Schothorst, C. Meplan, L. Schomburg, C. Evelo, S.L. Coort, S. Gaj, J. Keijer, J. Hesketh, R. Brigelius

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Abstract

Selenium is an essential micronutrient. Its recommended daily allowance is not attained by a significant proportion of the population in many countries and its intake has been suggested to affect colorectal carcinogenesis. Therefore, microarrays were used to determine how both selenoprotein and global gene expression patterns in the mouse colon were affected by marginal selenium deficiency comparable to variations in human dietary intakes. Two groups of 12 mice each were fed a selenium-deficient (0.086 mg Se/kg) or a selenium-adequate (0.15 mg Se/kg) diet. After 6 wk, plasma selenium level, liver, and colon glutathione peroxidase (GPx) activity in the deficient group was 12, 34, and 50%, respectively, of that of the adequate group. Differential gene expression was analysed with mouse 44K whole genome microarrays. Pathway analysis by GenMAPP identified the protein biosynthesis pathway as most significantly affected, followed by inflammation, Delta-Notch and Wnt pathways. Selected gene expression changes were confirmed by quantitative real-time PCR. GPx1 and the selenoproteins W, H, and M, responded significantly to selenium intake making them candidates as biomarkers for selenium status. Thus, feeding a marginal selenium-deficient diet resulted in distinct changes in global gene expression in the mouse colon. Modulation of cancer-related pathways may contribute to the higher susceptibility to colon carcinogenesis in low selenium status
Original languageEnglish
Pages (from-to)1561-1572
JournalMolecular Nutrition & Food Research
Volume53
Issue number12
DOIs
Publication statusPublished - 2009

Keywords

  • messenger-rna stability
  • thioredoxin-like family
  • glutathione-peroxidase
  • gene-expression
  • microarray data
  • colorectal adenoma
  • cancer prevention
  • molecular targets
  • oxidative stress
  • selenocysteine

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