大鼠缺铁：肌肉功能障碍的生理生化研究
Iron deficiency in the rat. Physiological and biochemical studies of muscle dysfunction.
作者信息
Finch C A, Miller L R, Inamdar A R, Person R, Seiler K, Mackler B
出版信息
J Clin Invest. 1976 Aug;58(2):447-53. doi: 10.1172/JCI108489.
Abstract
Work performance on a treadmill has been evaluated in normal and iron-deficient rats. Anemia was removed as a variable by adjusting the hemoglobin of all animals to the same concentration. At a hemoglobin compatible with normal work performance, iron-deficient animals showed a marked impairment of running ability as compared to control animals. Iron therapy corrected the disability within 4 days. Concentrations of the cytochrome pigments and myoglobin, and rates of oxidative phosphorylation with pyruvate-malate, succinate, and alpha-glycerophosphate as substrates were all reduced in mitochondrial preparations from skeletal muscle of iron-deficient rats, but only the rate of phosphorylation with alpha-glycerophosphate as substrate increased significantly and in parallel with the recovery in work performance of the iron-deficient rats treated with iron dextran.
摘要
已对正常大鼠和缺铁大鼠在跑步机上的工作表现进行了评估。通过将所有动物的血红蛋白调整至相同浓度，消除了贫血这一变量。在与正常工作表现相符的血红蛋白水平下，与对照动物相比，缺铁动物的跑步能力明显受损。铁疗法在4天内纠正了这种功能障碍。缺铁大鼠骨骼肌线粒体制剂中细胞色素色素和肌红蛋白的浓度，以及以丙酮酸 - 苹果酸、琥珀酸和α - 甘油磷酸为底物的氧化磷酸化速率均降低，但仅以α - 甘油磷酸为底物的磷酸化速率显著增加，且与用右旋糖酐铁治疗的缺铁大鼠工作表现的恢复情况平行。
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