Selenium and vitamin E deficiencies were studied as part of an evaluation o
f oxidant defenses in guinea pigs. Male guinea pigs (100-120 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 seve
re weakness of their extremities. No guinea pigs in the other diet groups d
eveloped weakness. Guinea pigs from each group were killed on d 37, Seleniu
m deficiency and vitamin E deficiency were verified by measurement of gluta
thione peroxidase and alpha -tocopherol. Creatine phophokinase (CPK) activi
ty was greater than controls in both groups fed vitamin E-deficient diets,
but the increase was greater in the 0 Se-0 E group than in the 0 E group. M
uscle F-2-isoprostanes were greater than controls in both groups fed vitami
n E-deficient 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 gro
up, minimal in the 0 E group and absent from other groups. The diets used i
n this study induced selenium and vitamin E deficiencies in guinea pigs. Th
e study demonstrates that combined selenium and vitamin E deficiency result
s in a fatal myopathy in guinea pigs that is associated with lipid peroxida
tion in the affected muscle. This nutritional myopathy is much more severe
than the myopathy that occurs with vitamin E deficiency alone.