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).

Bimodal actions of selenium essential for antioxidant and toxic pro-oxidant activities: The selenium paradox (Review)

“…Chronic exposure to high doses of dietary selenium in the range of milligrams per kilogram causes alkali diseases and blinder staggers in livestock that graze in pastures with selenium-rich soil (8,9). Since plants absorb selenium more easily when grown in alkali soil, alkali disease frequently occurs in livestock that feed on selenium-tolerant plants with high selenium levels ranging from 5 to 50 milligram per kilogram of mass.…”

“…However, a deficiency in selenium has been linked to many clinical symptoms including Kashin-Beck disease, which is characterized by bone and joint degeneration in children (6), and Keshan's disease that is known to cause cardiomyopathy in humans (1,7). Moreover, it is well known that an excessive intake of selenium results in toxic symptoms including alkaline disease and blind staggers in livestock (8,9). Selenium poisoning is thought to result from the generation of oxygen radicals that can lead to DNA damage, lipid peroxidation, and premature protein degradation inside the cell (10)(11)(12).…”

Differential gene expression in skeletal muscle of rats with Vitamin E deficiency

“…Occasional dystrophic calcification can also occur. Besides these alterations, signs of cellular regeneration including activated satellite cells and multinucleated myotubes are prominent (5).…”

Selenium status and associated factors in a British National Diet and Nutrition Survey: young people aged 4–18 y

“…In places where Se levels are very high, animals and plants may accumulate excessive amounts, thus posing a danger of toxicity to humans (van Vleet & Ferrans, 1992;Xia et al, 1992). Conversely, Se deficiency is also a well-established problem for farm animals and human populations in certain parts of the world, and is associated with pathological lesions and with undesirably low biochemical status values (Oldfield, 1999).…”