Selenium Intake Induces Growth Retardation Through Reversible Growth Hormone and Irreversible Somatomedin C Suppression
Growth retardation is an outstanding symptom in animals exposed to toxic doses of selenium and is one of the main symptoms in stocks with alkali disease. Even Moxon (1937) demonstrated a convincing correlation between the dose of selenium consumed by experimental animals and the level of growth retardation. These results have later been confirmed by many others and the National Research Council concluded in 1976 that growth retardation may be the best indicator of selenium toxicity. The mechanism behind this symptom has, however, not been clearly established although reduced food intake seems to be a part of this mechanism.
KeywordsPlacebo Toxicity Selenium Selenite Toxicology
Unable to display preview. Download preview PDF.
- Moxon AL (1937) Alkali disease or selenium poisoning. S D Agric Exp Stn Bull 311: 1–91Google Scholar
- National Research Council (1976) Selenium. Natl Acad Sci, Washington DC, pp 115–116Google Scholar
- Thorlacius-Ussing O, Flyvbjerg A, Damm Jorgensen K, Orskov H (1988a) Growth hormone restores normal growth in selenium-treated rats without increase in circulating somatomedin C. Acta Endocrinol (Copenh) 117: 65–72Google Scholar
- Thorlacius-Ussing O, Flyvbjerg A, (rskov H (1988b) Growth in young rats after termination of sodium selenite exposure: studies of growth hormone and somatomedin C. Toxicology 48: 167–176Google Scholar