Related Experiment Videos
Microarray analysis of selenium-depleted and selenium-supplemented mice.
L A Hooven1, J Butler, L W Ream
1Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331, USA.
Biological Trace Element Research
|January 31, 2006
Summary
Selenium deficiency in mice impacts gene expression in muscles, affecting immune and cellular pathways. Supplementation with sodium selenate partially restored normal gene activity, highlighting selenium
Area of Science:
- Nutritional biochemistry
- Molecular biology
- Genomics
Background:
- Nutritional selenium deficiency is linked to Keshan disease in humans and white muscle disease in livestock.
- Understanding selenium's role in gene expression is crucial for preventing related health issues.
Purpose of the Study:
- To investigate the effects of chronic selenium deficiency and repletion on gene expression in mouse muscle.
- To identify specific genes and pathways affected by selenium levels using DNA microarrays.
Main Methods:
- Mice were fed a selenium-deficient diet for three generations.
- Third-generation female mice received water with no added selenium, 0.1 ppm, or 1.0 ppm selenium as sodium selenate.
- DNA microarrays were employed to compare gene expression profiles in muscle tissue.
Main Results:
- Selenium repletion led to significant changes in gene expression.
- Upregulated genes included Ptger2, Tcrb-V13, Tcf-7, and Lck, involved in immune and cellular signaling.
- Vav2, a mouse oncogene, showed decreased expression with selenium-containing diets.
Conclusions:
- Chronic selenium deficiency alters muscle gene expression, impacting immune and cellular functions.
- Selenium repletion, particularly with sodium selenate, can modulate these gene expression patterns.
- Findings suggest a role for selenium in regulating specific oncogenes and immune-related genes.