Etiologic factors and pathologic alterations in selenium-vitamin E deficiency and excess in animals and humans.

Abstract

The etiology of selenium-vitamin E (Se-E) deficiency diseases may be complex. Many of the syndromes involve combined deficiency of selenium and vitamin E. Selenium moves into the animal and human food chain from soil and plants, which may contain inadequate amounts of the nutrient in many areas of the world. Vitamin E may be in low concentration in many animal feeds unless supplements are added. Some syndromes, such as steatitis in cats, result from an increased requirement of vitamin E in diets that contain large amounts of polyunsaturated fatty acids, and these diseases will only respond to vitamin E administration. Deficiency syndromes in animals owing to pure Se deficiency are infrequent and have been produced mainly by laboratory studies utilizing extreme deficiency conditions. Other factors that may affect the occurrence of these deficiency diseases are concurrent dietary deficiency of S-containing amino acids, bioavailability of different forms of dietary Se, intake of compounds that antagonize Se (e.g., silver salts), and exposure to various prooxidant substances (e.g., iron compounds, oxygen, ozone, and various drugs).

• Authors: J F Van Vleet, V J Ferrans
• Journal: Biological trace element research (Biol Trace Elem Res) 1992 Apr-Jun Vol. 33 Pg. 1-21 ISSN: 0163-4984 [Print] United States
• PMID: 1379446 (Publication Type: Journal Article, Review)

Chemical References

• Lipofuscin
• Vitamin E
• Selenium

Topics

• Animals
• Cardiomyopathies (etiology)
• Humans
• Lipofuscin (metabolism)
• Male
• Muscles (pathology)
• Muscular Diseases (etiology)
• Myocardium (pathology)
• Nervous System Diseases (etiology)
• Selenium (adverse effects, deficiency, toxicity)
• Vitamin E (adverse effects, toxicity)
• Vitamin E Deficiency (etiology, pathology)