Tanne Z, Coleman R, Nahir M, Shomrat D, Finberg J P, Youdim M B
Department of Pharmacology, Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa.
Biochem Pharmacol. 1994 May 18;47(10):1759-66. doi: 10.1016/0006-2952(94)90303-4.
Male Sprague-Dawley rats aged 3 weeks that were maintained on an iron-deficient diet for 4-5 weeks developed severe anemia with markedly reduced hemoglobin levels (3.94 +/- 0.14 Hb g% versus controls 12.9 +/- 0.11 Hb g%). Iron-deficiency resulted in marked cardiac hypertrophy (cardiomegaly). On sacrifice, the hearts were processed for light and transmission electron microscopy. The major ultrastructural changes were found in the hypertrophied left ventricle and left papillary muscles. Iron-deficiency caused marked edema in myocytes, sarcomeres were out of register, and degeneration and discontinuities in myofilaments were common. Iron-deficiency resulted in the enlargement of the interfibrillar mitochondria, changes in the matrix and the formation of electron-dense amorphous bodies. The ultrastructural changes in myocytes in response to experimental iron-deficiency were similar to those described by others in cases of experimental ischemia or hypoxia. Mitochondrial changes were also found in the atria of iron-deficient rats. Quantitative cytochemical measurement of succinate dehydrogenase activity was determined and was shown to be substantially reduced in the iron-deficient heart. In severely iron-deficient rats restored to a normal iron-sufficient diet for two weeks, hemoglobin levels recovered, however the myocytes of the hypertrophied left ventricles and papillary muscles continued to show severe degenerative changes.
3周龄的雄性斯普拉格-道利大鼠维持缺铁饮食4-5周后,出现严重贫血,血红蛋白水平显著降低(血红蛋白含量为3.94±0.14 g%,而对照组为12.9±0.11 g%)。缺铁导致明显的心脏肥大(心脏扩大)。处死大鼠后,取心脏进行光镜和透射电镜检查。主要超微结构变化见于肥厚的左心室和左乳头肌。缺铁导致心肌细胞明显水肿,肌节排列紊乱,肌丝变性和断裂常见。缺铁导致肌原纤维间线粒体增大、基质改变以及电子致密无定形小体形成。实验性缺铁时心肌细胞的超微结构变化与其他人描述的实验性缺血或缺氧情况下的变化相似。缺铁大鼠的心房也发现了线粒体变化。对琥珀酸脱氢酶活性进行了定量细胞化学测定,结果显示缺铁心脏中的该酶活性显著降低。在严重缺铁的大鼠恢复正常铁充足饮食两周后,血红蛋白水平恢复,但肥厚的左心室和乳头肌的心肌细胞仍继续显示严重的退行性变化。