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Divisions of Gastroenterology and Endocrinology, Department of Medicine and Clinical Nutrition Research Unit, Vanderbilt University School of Medicine, Nashville, TN 37232-2279
2To whom correspondence should be addressed. E-mail: kristina.hill{at}mcmail.vanderbilt.edu.
Selenium and vitamin E deficiencies were studied as part of an
evaluation of oxidant defenses in guinea pigs. Male guinea pigs
(100120 g) were fed a control diet (C) or the diet without selenium
(0 Se), without vitamin E (0 E), or without either selenium or vitamin
E (0 Se-0 E). Between d 30 and 35, 7 of 13 guinea pigs fed the 0 Se-0 E
diet were euthanized because of severe weakness of their extremities.
No guinea pigs in the other diet groups developed weakness. Guinea pigs
from each group were killed on d 37. Selenium deficiency and vitamin E
deficiency were verified by measurement of glutathione peroxidase and
-tocopherol. Creatine phophokinase (CPK) activity was greater than
controls in both groups fed vitamin Edeficient diets, but the
increase was greater in the 0 Se-0 E group than in the 0 E group.
Muscle F2-isoprostanes were greater than controls in both
groups fed vitamin Edeficient diets with the level in the 0 Se-0 E
group greater than that in the 0 E group. Histologic muscle necrosis
was severe in the 0 Se-0 E group, minimal in the 0 E group and absent
from other groups. The diets used in this study induced selenium and
vitamin E deficiencies in guinea pigs. The study demonstrates that
combined selenium and vitamin E deficiency results in a fatal myopathy
in guinea pigs that is associated with lipid peroxidation in the
affected muscle. This nutritional myopathy is much more severe than the
myopathy that occurs with vitamin E deficiency alone.
KEY WORDS: myopathy selenium vitamin E lipid peroxidation guinea pigs
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