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

Abstract

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,

Noninvasive Mapping of Reactive Oxygen Species by in Vivo Electron Spin Resonance Spectroscopy in Indomethacin-Induced Gastric Ulcers in Rats

“…(Utsumi et al, 1990). Hydroxy-TEMPO can easily permeate the membrane of cells and rapidly lose its paramagnetism by bioreduction such as enzymes in electron transport system (Quintanilha and Packer, 1977) and ascorbic acid (Perkins et al, 1980), whereas carbamoyl-PROXYL minimally permeates the cell membrane and is minimally reduced. On the other hand, in this study, the signal-decay rates of all tested probes administered orally to NaHCO 3 -treated rats at the gastric region were similar.…”

Avaliação dos efeitos da suplementação com ácidos ascórbicos sobre os aspectos morfoquantitativos do plexo mioentérico do jejuno de camundongos mdx com ausência de distrofina

“…Estudos experimentais sobre a DMD são desenvolvidos a partir da utilização de animais distróficos como cães da raça Golden Retriver, gatos, ratos, camundongos e aves (CARPENTER et al, 1989;GASGHEN et al, 1992;KORNEGAY et al, 2011;PUTTEN et al, 2012;PERKINS et al, 1980). Embora apresentem semelhanças nas características gerais da distrofia muscular, esses animais possuem diferentes capacidades de regeneração (SEIXAS et al, 1997 ROBIN;FALEWSKI, 1963;BENSEN;TARR, 1996), má absorção intestinal ONG;DRAKE, 1964), disfagia, vômito, constipação crônica (JAFFE et al, 1990 e pseudo-obstrução intestinal (LEON et al,1986).…”

“…Acredita-se que o processo degenerativo característico da DMD promova um aumento das concentrações de agentes deletérios, como os radicais livres, responsáveis pelo estresse oxidativo (PERKINS et al, 1980). Assim, com o intuito de atenuar ou mesmo erradicar esses efeitos, Perkins et al (1980) 1982;BAROHN et al, 1988;BENSEN;TARR, 1996).…”

“…Assim, com o intuito de atenuar ou mesmo erradicar esses efeitos, Perkins et al (1980) 1982;BAROHN et al, 1988;BENSEN;TARR, 1996). Autópsias realizadas após morte em pacientes com Distrofia muscular de Duchenne mostrou que ocorre substituição do tecido muscular liso por tecido conectivo e adiposo (HUVOS; PRUZANSKI, 1967).…”

“…Existem diversos modelos animais para o estudo da Distrófia Muscular de Duchenne (PERKINS et al, 1980, CARPENTER et al, 1989GASGHEN et al, 1992;KORNEGAY et al, 2011;PUTTEN et al, 2012). Para a utilização destes modelos, é crucial o conhecimento de suas características patológicas (WILLMANN, et al, 2009 A análise desses dados permitiu verificar que os animais distróficos (grupos GD30 e GD60) apresentaram peso corpóreo significativamente maior que seus respectivos controles (grupos GC30 e GC60) (p<0,05).…”