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

1958 ◽  
Vol 193 (3) ◽  
pp. 530-533 ◽  
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.

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

1959 ◽  
Vol 197 (2) ◽  
pp. 491-493 ◽  
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.

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

Blood ◽  
1978 ◽  
Vol 52 (1) ◽  
pp. 187-195 ◽  
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.

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

1960 ◽  
Vol 198 (6) ◽  
pp. 1232-1234 ◽  
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.

Production of Vitamin-E Deficiency and Muscular Dystrophy in Pigs

1961 ◽  
Vol 2 (1) ◽  
pp. 67-72 ◽  
Author(s):  
N. Lannek ◽  
P. Lindberg ◽  
G. Nilsson ◽  
G. Nordström ◽  
K. Orstadius
Keyword(s):  
Vitamin E ◽  
Muscular Dystrophy ◽  
Vitamin E Deficiency

Biochemical changes in progressive muscular dystrophy. XIII. Nucleic acids, proteins, and total nucleotides in the thymus and spleen of dystrophic mice

1985 ◽  
Vol 63 (5) ◽  
pp. 325-332 ◽  
Author(s):  
Uma Srivastava ◽  
Mikael Sebag ◽  
Manohar Thakur
Keyword(s):  
Skeletal Muscle ◽  
Amino Acid ◽  
Muscular Dystrophy ◽  
Free Amino Acid ◽  
Free Amino ◽  
Specific Activity ◽  
Cellular Growth ◽  
Free Amino Acid Pool ◽  
Acid Pool ◽  
Dystrophic Mice

Assessments were made of the thymus and spleen weights and the total nucleotide, nucleic acid, and protein content as well as the incorporation of [14C]leucine into protein and of [3H]orotate into RNA, in the thymus, spleen, liver, brain, kidney, lungs, heart, pancreas, and skeletal muscle of normal (+/+) and dystrophic (dy/dy) 129 ReJ mice aged 40, 60, or 90 days. The weights of the thymus and spleen were lower at all stages of dystrophy. Total nucleotide and RNA levels per thymus were reduced at 90 days, while total DNA content was decreased at 60 and 90 days. Protein concentrations per thymus were diminished at each stage of the disease. The specific activity of the free amino acid pool and total free nucleotide pool did not show any significant variations in the thymus at any phase of dystrophy. Incorporation of [14C]leucine into protein and of [3H]orotate into RNA was considerably lower in the thymus at each stage of the disease. Total nucleotide content per spleen was decreased at 40 days, with no change at 60 days and followed by an increase at 90 days in the dystrophic mice. DNA, RNA, and protein levels were all reduced in the spleen at each stage of the disease. The specific activity of the free amino acid pool and total free nucleotide pool, as well as the incorporation of [14C]leucine into protein and of [3H]orotate into RNA, showed similar changes in the spleen as noted in the thymus at each phase of dystrophy. These observations indicate that significant alterations in cellular growth occur not only in skeletal muscle and other nonlymphoid organs, but also in the lymphoid organs of dystrophic mice. Such changes in the cellular growth of lymphoid organs could be responsible for an impairment of immunologic responses reflecting thymic atrophy in murine muscular dystrophy.

scholarly journals Some Effects of Prolonged Vitamin E Deficiency in The Rat

1939 ◽  
Vol 39 (6) ◽  
pp. 643-652 ◽  
Author(s):  
Archer John Porter Martin ◽  
Thomas Moore
Keyword(s):  
Vitamin E ◽  
Muscular Dystrophy ◽  
Skeletal Muscles ◽  
Vitamin E Deficiency ◽  
Leg Muscles ◽  
Brown Discoloration ◽  
Recent Developments ◽  
Preliminary Communication ◽  
Convoluted Tubules ◽  
Nutritional Muscular Dystrophy

IN an early preliminary communication we (Martin & Moore, 1936) reported that in rats maintained for prolonged periods on diets deficient in vitamin E a brown discoloration of the uterus occurred. Degeneration of the convoluted tubules of the kidneys was also found. In a more recent paper we (Martin & Moore, 1938) described a less intense discoloration in the skeletal muscles, which was localized in distribution. The muscles of the hindlegs, which displayed the paresis described by Ringsted (1935), were always noticeably discoloured. In both the uterine and leg muscles discoloration was found to be associated with muscular degeneration. The similarity of the condition in the leg muscles to the nutritional muscular dystrophy first reported by Goettsch & Pappenheimer (1931) in guinea-pigs was noted. The purpose of this communication is to give a detailed account of this work, including its most recent developments (Moore, 1939).

scholarly journals Reversal of cardiac and skeletal manifestations of Duchenne muscular dystrophy by cardiosphere-derived cells and their exosomes in mdx dystrophic mice and in human Duchenne cardiomyocytes

2017 ◽  
Author(s):  
Mark A. Aminzadeh ◽  
Russell G. Rogers ◽  
Kenneth Gouin ◽  
Mario Fournier ◽  
Rachel E. Tobin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Mouse Model ◽  
Cardiac Function ◽  
Premature Death ◽  
Next Generation ◽  
Skeletal Myopathy ◽  
Genetic Deficiency ◽  
Dystrophic Mice

Genetic deficiency of dystrophin leads to disability and premature death in Duchenne muscular dystrophy, affecting the heart as well as skeletal muscle. Here we report that cardiosphere-derived cells (CDCs), which are being tested clinically for the treatment of Duchenne cardiomyopathy, improve cardiac and skeletal myopathy in the mdx mouse model of DMD and in human Duchenne cardiomyocytes. Injection of CDCs into the hearts of mdx mice augments cardiac function, ambulatory capacity and survival. Exosomes secreted by human CDCs reproduce the benefits of CDCs in mdx mice and in human Duchenne cardiomyocytes. The findings further motivate the testing of CDCs in Duchenne patients, while identifying exosomes as next-generation therapeutic candidates.

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