Vitamin e deficiency is rare but it leads to oxidative damage of the cell membranes leading to the development of myopathic and neurological disorders
Answers
Vitamin E Deficiency
Vitamin E deficiency can result from severe fat malabsorption with consequent steatorrhea, some forms of cholestatic liver disease, abetalipoproteinemia, and intestinal resection. In experimental animals vitamin E deficiency has resulted in fetal resorption, premature infants have been born with inadequate reserves, and in males testicular atrophy has occurred.
Excessive lipid peroxidation of membranes and other sites of fat accumulation accounts for most of the symptoms associated with vitamin E deficiency. The most clear-cut example is enhanced erythrocyte fragility, where RBCs exhibit a marked change in morphology and become easily destroyed. Vitamin E is also essential for the development and maintenance of normal nerve and muscle cell activity. Either vitamin E or selenium deficiency can result in a massive influx of Ca++ into cells; mitochondria become loaded with this element, and reduce their ATP output. This mineral influx results in muscular degeneration, and gives muscle a characteristic appearance (i.e., “white muscle disease”), which is usually more prominent in young animals. Myocardial involvement with this disease may result in sudden death.
White muscle disease is sometimes confused with the muscular dystrophies of animals, which are hereditary degenerative diseases of skeletal muscle. Dystrophic muscles usually contain fewer fibers, an increase in the number and size of nuclei, and myofibrillar degeneration without effective regeneration.
Another outcome of the lack of antioxidant action of vitamin E, and which occurs in its deficiency, is the accumulation of “lipofuscin” or “ceroid pigment” granules in many tissues, including the CNS, lungs, kidneys, adipocytes, and muscle. These granules contain oxidized unmetabolizable lipids that have partially crosslinked with protein or peptides to form a hard globule that cannot be disposed of by the organism. These granules normally accumulate with age, and this accumulation is inhibited by a high vitamin E intake, at least in mice. Fatty tissue inflammation (i.e., “steatitis”), is also associated with vitamin E deficiency.
Animals with cholestasis (e.g., bile duct obstruction) absorb fat-soluble vitamins poorly. In chronic conditions neuromuscular damage occurs that can be somewhat alleviated through parenteral administration of vitamin E. Additionally, retinopathy can occur in vitamin E deficiency upon exposure to high oxygen tensions. Again, this condition has been reversed with vitamin E administration.
Studies in several animal species have shown that in males, vitamin E deficiency results first in sperm immotility, then in degeneration of the seminiferous epithelium, and then cessation of sperm production. In females there is a failure of uterine function in vitamin E deficiency, with a lack of development of the vasculature that would allow the conceptus to implant in the uterine wall. Although vitamin E supplementation can help to reverse these symptoms, Se does not effectively prevent fetal resorption in rats, nor encephalomalacia in chickens, and thus, is not a complete substitute for vitamin E.
Although several health problems have been associated with vitamin E deficiency, as discussed above, high intakes of this vitamin do not appear to be as debilitating as do those for vitamins A, D and K. Vitamin E, however, can act as an anticoagulant, therefore hypervitaminosis E may increase the risk of bleeding.
Vitamin E Deficiency
Vitamin E deficiency can result from severe fat malabsorption with consequent steatorrhea, some forms of cholestatic liver disease, abetalipoproteinemia, and intestinal resection. In experimental animals vitamin E deficiency has resulted in fetal resorption, premature infants have been born with inadequate reserves, and in males testicular atrophy has occurred.
Excessive lipid peroxidation of membranes and other sites of fat accumulation accounts for most of the symptoms associated with vitamin E deficiency. The most clear-cut example is enhanced erythrocyte fragility, where RBCs exhibit a marked change in morphology and become easily destroyed. Vitamin E is also essential for the development and maintenance of normal nerve and muscle cell activity. Either vitamin E or selenium deficiency can result in a massive influx of Ca++ into cells; mitochondria become loaded with this element, and reduce their ATP output. This mineral influx results in muscular degeneration, and gives muscle a characteristic appearance (i.e., “white muscle disease”), which is usually more prominent in young animals. Myocardial involvement with this disease may result in sudden death.
White muscle disease is sometimes confused with the muscular dystrophies of animals, which are hereditary degenerative diseases of skeletal muscle. Dystrophic muscles usually contain fewer fibers, an increase in the number and size of nuclei, and myofibrillar degeneration without effective regeneration.
Another outcome of the lack of antioxidant action of vitamin E, and which occurs in its deficiency, is the accumulation of “lipofuscin” or “ceroid pigment” granules in many tissues, including the CNS, lungs, kidneys, adipocytes, and muscle. These granules contain oxidized unmetabolizable lipids that have partially crosslinked with protein or peptides to form a hard globule that cannot be disposed of by the organism. These granules normally accumulate with age, and this accumulation is inhibited by a high vitamin E intake, at least in mice. Fatty tissue inflammation (i.e., “steatitis”), is also associated with vitamin E deficiency.
Animals with cholestasis (e.g., bile duct obstruction) absorb fat-soluble vitamins poorly. In chronic conditions neuromuscular damage occurs that can be somewhat alleviated through parenteral administration of vitamin E. Additionally, retinopathy can occur in vitamin E deficiency upon exposure to high oxygen tensions. Again, this condition has been reversed with vitamin E administration.
Studies in several animal species have shown that in males, vitamin E deficiency results first in sperm immotility, then in degeneration of the seminiferous epithelium, and then cessation of sperm production. In females there is a failure of uterine function in vitamin E deficiency, with a lack of development of the vasculature that would allow the conceptus to implant in the uterine wall. Although vitamin E supplementation can help to reverse these symptoms, Se does not effectively prevent fetal resorption in rats, nor encephalomalacia in chickens, and thus, is not a complete substitute for vitamin E.
Although several health problems have been associated with vitamin E deficiency, as discussed above, high intakes of this vitamin do not appear to be as debilitating as do those for vitamins A, D and K. Vitamin E, however, can act as an anticoagulant, therefore hypervitaminosis E may increase the risk of bleeding.