Free Amino Acids of Developing Skeletal Musculature of Normal and Genetically Dystrophic Chickens.

Wilson, Barry W.; Peterson, D. W.; Lilyblade, A. L.

doi:10.3181/00379727-119-30109

Cited by 28 publications

(7 citation statements)

References 1 publication

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“…The data in this paper, taken together with the results of others (3,4,(8)(9)(10), offer supportive evidence for involvement of the intracellular redox status in the pathogenesis of avian muscular dystrophy.…”

Section: Methodssupporting

confidence: 84%

“…If dystrophic muscle were capable of an induced synthesis of enzymes in response to free radicals and peroxides, it seemed possible that dystrophic muscle might also accumulate smallmolecule antioxidants to facilitate removal of excess damaging free radicals. In fact, the levels of reduced and oxidized glutathione are elevated in muscles of dystrophic chickens and mice (9)(10)(11).…”

mentioning

confidence: 99%

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Enhancement of free radical reduction by elevated concentrations of ascorbic acid in avian dystrophic muscle.

Perkins¹,

Beth²,

Wilkerson³

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

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It has been postulated that the degenerative process in dystrophic muscle results from increased concentrations of free radicals, eroxides, or lipid hydroperoxides. Therefore, the reduction of the free radical tanol (2,2,6,6-tetramethyl-4-iperidinol-1-oxyl) by extracts of muscles of dystrophic and normal chickens was studied. Pectoral (white) and thigh (red) muscles were used. For initial rate measurements, the various muscle extracts were added to an equal volume of 0.2 mM tanol. Reaction mixtures were introduced into the EPR cavity in a standard aqueous flat cell. Rates were measured by continuously monitoring the decrease in signal amplitude of the center (MI = 0) solution tanol EPR resonance line (in-phase first harmonic absorption signal). With extracts from dystrophic white muscle, the reduction rate was 75% faster than normal, whereas in dystrophic red muscle extracts the rate was normal. This agreed with previous observations that white muscle is more severely affected than red in dystrophic chickens. The primary reductant was identified as reduced ascorbic acid, and the rate of reduction of tanol correlated directly with the concentrations of ascorbic acid in the various muscle extracts as shown by chemical analysis. The results suggest an involvement of the intracellular redox status in the pathogenesis of avian muscular dystrophy. Avian (chicken) muscular dystrophy has been considered as a model for human muscular dystrophy, in particular Duchenne dystrophy (1). Avian dystrophy is characterized: (i) by muscle weakness and atrophy, which is apparent when the bird is placed on its back and cannot right itself; (ii) by contractures or stiffness of the wings, which cannot be elevated beyond a horizontal plane; and (iii) biochemically, by increased levels of muscle enzymes in the serum, for example, creatine kinase and aldolase (1). The chicken is a good model because of the natural anatomical separation of the white, fast fibers (pectoral) and red, slow fibers (thigh and gastrocnemius). In avian and Duchenne dystrophy, the white muscle fibers are much more severely affected than the red (1, 2).It has been postulated that the degenerative process in dystrophic muscle may result from increased concentrations of deleterious agents such as free radicals, peroxides, and lipid hydroperoxides (3, 4). These agents promote lipid peroxidation,

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Section: Methodssupporting

confidence: 84%

mentioning

confidence: 99%

Enhancement of free radical reduction by elevated concentrations of ascorbic acid in avian dystrophic muscle.

Perkins¹,

Beth²,

Wilkerson³

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

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“…Taurine has been shown to increase from 33 to 126 mmoledkg dry weight in experimentally induced congestive heart failure") and to be elevated in heart tissue of humans who died of chronic congestive heart failure."' Wilson et al 43 reported taurine and glutathione concentrations to be elevated in skeletal muscle of dystrophic chickens, and the taurine levels increased with age. Baskin and Dagirmanjian' suggested that increases in taurine might be the biochemical basis of the lesions caused by muscular dystrophy.…”

Section: Resultsmentioning

confidence: 99%

Intracellular elemental content of cardiac and skeletal muscle of normal and dystrophic hamsters

et al. 1983

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To test the hypothesis that the genetic lesion causing muscular dystrophy might be reflected in an abnormal intracellular elemental content, the elemental content of individual cardiac and skeletal muscle fibers in 50-day-old male control and cardiomyopathic BIO 53.58 hamsters was determined. The technique of electron probe x-ray microanalysis of freeze-dried tissue was employed. No electrolyte content differences were found between control and diseased animals for nuclei, myofibrillar cytoplasm, or mitochondrially-enriched cytoplasm of cardiac myocytes. Sulfur was elevated in dystrophic cardiac myocytes and was the only element significantly different in heart tissue of control and cardiomyopathic animals. Sulfur was also elevated in dystrophic soleus muscle fibers. The pattern of electrolyte content of these cells reflected a mixture of normal cells and damaged cells with altered electrolyte content. In this hamster model, alteration of electrolyte content of myocytes appears to be a result of the disease process and not an inherent characteristic of muscular dystrophy. The elevated sulfur in dystrophic hamster myocytes reflects a biochemical lesion which deserves further study.

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“…Taurine content of muscles is higher in the embryo than in the 2-to 3-wk-old chick (Wilson et al, 1965). The concentration of taurine in the heart of the chick embryo increases gradually from the 7th d of incubation to the day of hatch, and remains constant in the adult.…”

Section: Introductionmentioning

confidence: 90%

Effects of Dietary Taurine on Growth and Escherichia coli Resistance in Chickens

Dunnington¹,

Siegel²,

Stewart

1996

Poultry Science

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White Leghorn chicks selected for either high (HA) or low (LA) antibody response to SRBC were used in two experiments to ascertain the effects of differing levels of dietary taurine on growth, levels of taurine in blood plasma, heart, and brain, and response to Escherichia coli inoculation. A different level of dietary taurine was associated with maximal growth in each of the two selected populations. Line HA expressed greater growth with a relatively low level of taurine, whereas Line LA expressed greater growth with a relatively high level of taurine. Line LA chicks had a higher level of taurine in the heart than did Line HA chicks. Although increases in dietary taurine resulted in linear and curvilinear increases in plasma and heart taurine levels, they had no effect on brain levels. No apparent resistance or susceptibility to E. coli exposure was associated with stock or differing levels of dietary taurine.

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Free Amino Acids of Developing Skeletal Musculature of Normal and Genetically Dystrophic Chickens.

Cited by 28 publications

References 1 publication

Enhancement of free radical reduction by elevated concentrations of ascorbic acid in avian dystrophic muscle.

Enhancement of free radical reduction by elevated concentrations of ascorbic acid in avian dystrophic muscle.

Intracellular elemental content of cardiac and skeletal muscle of normal and dystrophic hamsters

Effects of Dietary Taurine on Growth and Escherichia coli Resistance in Chickens

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