PATTERN OF IRON STORAGE IN THE RAT-HEART FOLLOWING IRON OVERLOADING WITH TRIMETHYLHEXANOYL-FERROCENE

Female Wistar rats with slight iron deficiency anemia were kept on a d iet containing 0.5% trimethylhexanoyl (TMH)-ferrocene for up to 79 wee ks. In the state of iron deficiency, the heart was free of light-micro scopically detectable iron. After 7 weeks of the TMH-ferrocene diet, t he 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 molec ules in the cytosol, and partly in lysosomes in the form of ferritin a nd/or hemosiderin. After 11 weeks, further iron-positive cells with re latively small dark-blue granules were found in the vicinity of capill aries, which could be identified as fibrocytes by means of electron mi croscopy. In addition, slight iron deposition occurred in the endothel ial cells of the cardiac capillaries, likewise mainly in the form of s mall, uniform siderosomes. The myocytes showed no product of Perls' Pr ussian blue reaction during the whole period of investigation. From th e 11th week onwards, discrete ferritin molecules were detected electro n microscopically within lysosomes of these cells. Their amount increa sed slowly with progression of the TMH-ferrocene feeding period. Free ferritin molecules could be observed in the cytosol of fibrocytes, end othelial cells and myocytes in only very slight concentrations, whilst they were more plentiful in macrophages. In hereditary hemochromatosi s 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.