Effect of vitamin E deficiency on creatine phosphokinase of heart and skeletal muscle

A quantitative determination of creatine phosphokinase activity of heart and skeletal muscle has been made in early and severe vitamin E deficiency in the rabbit. This study revealed that early vitamin E deficiency resulted in an increase in creatine phosphokinase activity of skeletal muscle but decreased the enzymatic activity of the heart. Severe vitamin E deficiency resulted in a decrease in creatine phosphokinase activity of both skeletal and heart muscle. 17-Hydroxycorticosterone, in small doses, resulted in an increase in enzymatic activity of skeletal muscle but no change in heart muscle. Large doses of 17-hydroxycorticosterone caused a decrease in the creatine phosphokinase activity of both heart and skeletal muscle. Normal male rabbits exhibited a lower enzymatic activity than female animals, a difference which, in part, was due to testosterone.

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6.3 The Development and Effects of Selenium Deficiency

BSAP Occasional Publication ◽

10.1017/s0263967x00030172 ◽

1983 ◽

Vol 7 ◽

pp. 128-128

Author(s):

J. R. Arthur ◽

R. Boyne

Keyword(s):

Skeletal Muscle ◽

Vitamin E ◽

Glutathione Peroxidase ◽

Heart Muscle ◽

Clinical Symptoms ◽

Selenium Deficiency ◽

Focal Lesions ◽

Vitamin E Deficiency ◽

Vitamin E Status ◽

Cattle And Sheep

Deficiencies of selenium (Se) and vitamin E can result in myopathies in cattle and sheep but the mechanics have not been clearly described. Both Se, as a component of the enzyme glutathione peroxidase, and vitamin E as a radicle scavenger, are involved in the protection of cells against the toxic effects of oxygen. In young calves, Se/vitamin E deficiency can result in the death of the animals due to a focal myopathy occurring in heart muscle; focal lesions are also found in skeletal muscle. In older calves, a more diffuse myopathy is usually confined to skeletal muscle and usually occurs when cattle are turned out from winter housing to spring pasture. However, low Se/vitamin E status will not invariably result in clinical symptoms of myopathy and other factors may be involved. This report describes some of the biochemical changes which can occur during the onset of clinical myopathy in Se/vitamin E-deficient cattle.

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Effect of short-term vitamin E deficiency on guinea pig skeletal muscle myoglobin

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1959.197.2.491 ◽

1959 ◽

Vol 197 (2) ◽

pp. 491-493 ◽

Cited By ~ 4

Author(s):

A. D. Bender ◽

D. D. Schottelius ◽

B. A. Schottelius

Keyword(s):

Skeletal Muscle ◽

Vitamin E ◽

Guinea Pig ◽

Guinea Pigs ◽

Short Term ◽

Vitamin E Deficiency ◽

Deficient Diet ◽

Wet Weight ◽

Masseter Muscles ◽

Nitrogen Percentage

Myoglobin concentration was determined in gastrocnemius and masseter muscles of guinea pigs maintained up to 15 days on vitamin E-deficient and vitamin E-supplemented diets. A statistically significant increase in myoglobin was noted in muscles of animals on the deficient diet for 15 days. That the increase was real and not apparent was attested by studies of total nitrogen, noncollagen nitrogen, percentage of solids and muscle wet weight, all of which were the same in control and experimental muscles. Histological sections and creatine excretion studies confirmed the impression of mild, incipient nutritional dystrophy.

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Severe Vitamin E deficiency exacerbates acute hyperoxic lung injury associated with increased oxidative stress and inflammation

Free Radical Research ◽

10.1080/10715760802189864 ◽

2008 ◽

Vol 42 (6) ◽

pp. 602-612 ◽

Cited By ~ 27

Author(s):

Shigeo Yamaoka ◽

Han-Suk Kim ◽

Tohru Ogihara ◽

Shinya Oue ◽

Kimitaka Takitani ◽

...

Keyword(s):

Oxidative Stress ◽

Vitamin E ◽

Lung Injury ◽

Vitamin E Deficiency ◽

Severe Vitamin ◽

Hyperoxic Lung Injury

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Abnormalities of iron metabolism and erythropoiesis in vitamin E- deficient rabbits

Blood ◽

10.1182/blood.v52.1.187.187 ◽

1978 ◽

Vol 52 (1) ◽

pp. 187-195 ◽

Cited By ~ 10

Author(s):

AC Chou ◽

GO Jr Broun ◽

CD Fitch

Keyword(s):

Skeletal Muscle ◽

Bone Marrow ◽

Vitamin E ◽

Iron Metabolism ◽

Iron Absorption ◽

Iron Concentration ◽

Vitamin E Deficiency ◽

Deficient Diet ◽

Plasma Iron ◽

Erythroid Hyperplasia

Abstract Rabbits fed a vitamin E-deficient diet developed severe muscular dystrophy in 3–4 wk, but they did not become anemic. Nevertheless, reticulocyte counts increased in deficient rabbits (3.2%) compared to control rabbits (0.9%), and erythroid hyperplasia was evident in the bone marrow. Comparing deficient rabbits to controls, the plasma iron concentration was lower (134.4 versus 206.6 microgram/dl); the TIBC was higher (335.9 versus 228.3 microgram/dl); the whole blood protoporphyrin concentration was higher (131.6 versus 81.7 microgram/dl); and the total iron content was lower in spleen (71 versus 153 microgram), higher in skeletal muscle (4956 versus 3054 microgram), and unchanged in bone marrow, liver, and heart. Studies of iron absorption and excretion using 59Fe showed no abnormalities in deficient rabbits. There were abnormalities of ferrokinetics, however. The half-time of disappearance of 59Fe was shorter (100.6 versus 169.4 min), the plasma iron turnover was greater (1.25 versus 0.95 mg/dl blood/day), and the reappearance of 59Fe in circulating erythrocytes at day 9 was greater (77.2% versus 57.2%) in deficient rabbits. Anemia induced by phlebotomy accentuated the abnormal iron metabolism of deficient rabbits, and the animals were unable to correct the anemia. These findings show that vitamin E deficiency in rabbits causes abnormal erythropoiesis associated with abnormal iron metabolism and sequestration of iron in skeletal muscle.

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Effect of Vitamin E-Deficiency on Protein Synthesis in Skeletal Muscle of the Rabbit.

Experimental Biology and Medicine ◽

10.3181/00379727-109-27085 ◽

1962 ◽

Vol 109 (1) ◽

pp. 8-10 ◽

Cited By ~ 1

Author(s):

J. F. Diehl ◽

L. L. Sanders

Keyword(s):

Skeletal Muscle ◽

Protein Synthesis ◽

Vitamin E ◽

Vitamin E Deficiency

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Metabolism of creatine-1-C14 by vitamin E-deficient and hyperthyroid rats

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1960.198.6.1232 ◽

1960 ◽

Vol 198 (6) ◽

pp. 1232-1234 ◽

Cited By ~ 15

Author(s):

Coy D. Fitch ◽

Randle Coker ◽

James S. Dinning

Keyword(s):

Skeletal Muscle ◽

Vitamin E ◽

Elevated Serum ◽

Vitamin E Deficiency ◽

Normal Vitamin

Normal, vitamin E-deficient and hyperthyroid rats were given creatine-1-C14 intraperitoneally, and its incorporation into skeletal muscle was determined. The incorporation of the creatine into skeletal muscle was increased in vitamin E-deficient rats while serum creatine-C14 activity was reduced. Hyperthyroidism led to a decreased incorporation of creatine into skeletal muscle and to elevated serum creatine-C14 levels. It is concluded that in vitamin E deficiency there is an inability of skeletal muscle to retain creatine and that in hyperthyroidism there is a block in the entry of creatine into skeletal muscle.

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Concentrations of K and Na in Skeletal Muscle of Mice With a Hereditary Myopathy (Dystrophia Muscularis)

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1958.193.3.530 ◽

1958 ◽

Vol 193 (3) ◽

pp. 530-533 ◽

Cited By ~ 27

Author(s):

Nome Baker ◽

William H. Blahd ◽

P. Hart

Keyword(s):

Skeletal Muscle ◽

Vitamin E ◽

Muscular Dystrophy ◽

Extracellular Space ◽

Partial Replacement ◽

Vitamin E Deficiency ◽

Normal Value ◽

Hereditary Myopathy ◽

The Mean ◽

Dystrophic Mice

Exchangeable body potassium (Ke), muscle potassium and muscle sodium concentrations have been measured in hereditarily dystrophic mice and in their normal littermates. Both Ke and K39/gm muscle were depressed in the dystrophics approximately 20% below the mean normal value; however, the concentration of Na23/gm muscle was higher by 50%, on the average, in the dystrophic tissue. The data suggest a partial replacement of intracellular by extracellular space in the dystrophic mice. Thus, this form of hereditary muscular dystrophy is qualitatively similar, with regard to K and Na concentrations, to human muscular dystrophy, vitamin E deficiency in rabbits, nutritional dystrophy in calves, and denervation in puppies.

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