Braumann A, Wulfhekel U, Nielsen P, Balkenhol B, Düllmann J
Anatomisches Institut, Universität Bonn, Deutschland.
Acta Anat (Basel). 1994;150(1):45-54. doi: 10.1159/000147601.
Female Wistar rats with slight iron deficiency anemia were kept on a diet containing 0.5% trimethylhexanoyl (TMH)-ferrocene for up to 79 weeks. In the state of iron deficiency, the heart was free of light-microscopically detectable iron. After 7 weeks of the TMH-ferrocene diet, the first iron-positive granules appeared in perivascular macrophages. Further oral administration caused a progression of iron deposition in these cells, visible in the form of a granular staining but also as a diffuse iron staining of the cytoplasm. Accordingly, at the electron-microscopical level, the iron was stored partly as free ferritin molecules in the cytosol, and partly in lysosomes in the form of ferritin and/or hemosiderin. After 11 weeks, further iron-positive cells with relatively small dark-blue granules were found in the vicinity of capillaries, which could be identified as fibrocytes by means of electron microscopy. In addition, slight iron deposition occurred in the endothelial cells of the cardiac capillaries, likewise mainly in the form of small, uniform siderosomes. The myocytes showed no product of Perls' Prussian blue reaction during the whole period of investigation. From the 11th week onwards, discrete ferritin molecules were detected electron microscopically within lysosomes of these cells. Their amount increased slowly with progression of the TMH-ferrocene feeding period. Free ferritin molecules could be observed in the cytosol of fibrocytes, endothelial cells and myocytes in only very slight concentrations, whilst they were more plentiful in macrophages. In hereditary hemochromatosis and posttransfusional siderosis, the iron is found predominantly in myocytes and appears to cause cell damage, whilst this is not the case in experimental iron overload in rats.
将轻度缺铁性贫血的雌性Wistar大鼠置于含0.5%三甲基己酰基（TMH）-二茂铁的饮食中长达79周。在缺铁状态下，心脏在光学显微镜下未检测到铁。在给予TMH-二茂铁饮食7周后，血管周围巨噬细胞中首次出现铁阳性颗粒。进一步口服给药导致这些细胞中铁沉积增加，表现为颗粒状染色，也表现为细胞质的弥漫性铁染色。相应地，在电子显微镜水平上，铁部分以游离铁蛋白分子的形式储存在细胞质中，部分以铁蛋白和/或含铁血黄素的形式储存在溶酶体中。11周后，在毛细血管附近发现了更多带有相对较小深蓝色颗粒的铁阳性细胞，通过电子显微镜可将其鉴定为成纤维细胞。此外，心脏毛细血管内皮细胞中也有轻微的铁沉积，同样主要以小的、均匀的含铁小体形式存在。在整个研究期间，心肌细胞未显示普鲁士蓝反应产物。从第11周起，在这些细胞的溶酶体内通过电子显微镜检测到离散的铁蛋白分子。随着TMH-二茂铁喂养期的延长，它们的数量缓慢增加。在成纤维细胞、内皮细胞和心肌细胞的细胞质中仅能观察到极少量的游离铁蛋白分子，而在巨噬细胞中则更为丰富。在遗传性血色素沉着症和输血后铁沉着症中，铁主要存在于心肌细胞中，似乎会导致细胞损伤，而在大鼠实验性铁过载中情况并非如此。
