Thompson C H, Green Y S, Ledingham J G, Radda G K, Rajagopalan B
Medical Research Council Biochemical and Clinical Magnetic Resonance Unit, John Radcliffe Hospital, Oxford, United Kingdom.
Acta Physiol Scand. 1993 Jan;147(1):85-90. doi: 10.1111/j.1748-1716.1993.tb09475.x.
Using 31P magnetic resonance spectroscopy we compared skeletal muscle bioenergetics in Wistar rats made chronically anaemic by being fed a diet deficient in iron for 6 weeks with chronically iron deficient animals given a normal diet as well as 5 mg iron dextran at 2 or 7 days before experimentation. Spectra of the gastrocnemius muscle were taken at rest and during stimulation of the sciatic nerve at 2 Hz for 10 min. Relative concentrations of intracellular phosphate (Pi), phosphocreatine (PCr) and ATP were determined. Iron deficiency increased PCr breakdown and production of acid in stimulated skeletal muscle. Recovery of PCr and Pi concentrations after exercise was slow. These metabolic changes are consistent with either a reduction in supply of oxygen to the muscle cell or altered oxidative phosphorylation by the mitochondria. The latter may be mediated by defective function of iron-containing proteins crucial in oxidative phosphorylation and this is suggested both by the observation that treatment with iron, sufficient to correct the anaemia, does not completely reverse the metabolic changes and that there is a different time course for such metabolic improvements and the observed increase in haemoglobin concentration.
我们使用31P磁共振波谱法,比较了通过喂食缺铁饮食6周而导致慢性贫血的Wistar大鼠、给予正常饮食以及在实验前2天或7天给予5毫克葡聚糖铁的慢性缺铁动物的骨骼肌生物能量学。在静息状态下以及在以2赫兹刺激坐骨神经10分钟期间,采集腓肠肌的波谱。测定细胞内磷酸盐(Pi)、磷酸肌酸(PCr)和三磷酸腺苷(ATP)的相对浓度。缺铁增加了受刺激骨骼肌中PCr的分解和酸的产生。运动后PCr和Pi浓度的恢复缓慢。这些代谢变化与肌肉细胞氧气供应减少或线粒体氧化磷酸化改变一致。后者可能由氧化磷酸化中关键的含铁蛋白质功能缺陷介导,这一点由以下观察结果表明:用足以纠正贫血的铁进行治疗并不能完全逆转代谢变化,而且这种代谢改善与观察到的血红蛋白浓度增加存在不同的时间进程。