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.
复制标题
通过提高禽类营养不良性肌肉中抗坏血酸的浓度来增强自由基的减少。
DOI：
10.1073/pnas.77.2.790
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发表时间：
1980
影响因子：
11.1
通讯作者：
J. H. Park
中科院分区：
文献类型：
--
作者：
R. C. Perkins;A. Beth;L. S. Wilkerson;W. Serafin;L. Dalton;C. R. Park;J. H. Park
据推测，营养不良性肌肉的退化过程是由自由基、过氧化物或脂质氢过氧化物浓度增加引起的。因此，研究了营养不良鸡和正常鸡的肌肉提取物对自由基三醇（2,2,6,6-四甲基-4-哌啶醇-1-氧基）的还原作用。使用胸肌（白色）和大腿（红色）肌肉。对于初始速率测量，将各种肌肉提取物添加到等体积的 0.2 mM tanol 中。将反应混合物引入标准水性扁平池的 EPR 腔中。通过连续监测中心 (MI = 0) 溶液 tanol EPR 共振线 (同相第一谐波吸收信号) 信号幅度的下降来测量速率。对于营养不良的白肌提取物，减少率比正常情况快 75%，而在营养不良的红肌提取物中，减少率正常。这与之前的观察一致，即营养不良鸡的白色肌肉比红色肌肉受到的影响更严重。主要还原剂被确定为还原的抗坏血酸，并且化学分析显示，三醇的还原速率与各种肌肉提取物中的抗坏血酸浓度直接相关。结果表明细胞内氧化还原状态参与禽类肌营养不良症的发病机制。
It has been postulated that the degenerative process in dystrophic muscle results from increased concentrations of free radicals, peroxides, or lipid hydroperoxides. Therefore, the reduction of the free radical tanol (2,2,6,6-tetramethyl-4-piperidinol-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.