TY - JOUR
T1 - Ultrastructural pathology of iron-loaded rat myocardial cells in culture
AU - Iancu, T. C.
AU - Shiloh, H.
AU - Link, G.
AU - Bauminger, E. R.
AU - Pinson, A.
AU - Hershko, C.
PY - 1987
Y1 - 1987
N2 - The pathological changes induced by in-vitro iron-loading or cultured rat myocardial cells were studied. Cells were exposed to 59Fe-labelled ferric ammonium citrate for up to 24 h followed by 24-72 h chase experiment. After 24 h exposure 29% of the total cellular radioactivity was found in ferritin. 10% in non-ferritin heat supernatant and 61% in an insoluble heat-precipitable form. Mossbauer spectroscopy showed a gradual shift from intracellular iron particles less than 1.8 nm in diameter, through particles of intermediate size, to ferritin-like aggregates over 3.0 nm in diameter, reaching about 20% of total iron by 24 h. Ultrastructural studies showed premature damage such as mitochondrial abnormalities and excessive autophagocytosis. Small, 2.0-5.0 nm electron-dense cytosolic particles were noticed at 3 h of iron loading and reached maximal concentrations at 6 h. This was followed by accumulation of the small particles and of typical iron-rich ferritin cores within siderosomes. Because of the limited duration of iron loading and the high concentrations of non-transferrin inorganic iron employed, the present model is more relevant to acute than chronic iron overload. The efficient incorporation of large amounts of iron within ferritin molecules and its subsequent segregation, together with other smaller particles, within membrane-bound bodies, may represent a defence mechanism limiting iron toxicity in the face of advanced cytosiderosis.
AB - The pathological changes induced by in-vitro iron-loading or cultured rat myocardial cells were studied. Cells were exposed to 59Fe-labelled ferric ammonium citrate for up to 24 h followed by 24-72 h chase experiment. After 24 h exposure 29% of the total cellular radioactivity was found in ferritin. 10% in non-ferritin heat supernatant and 61% in an insoluble heat-precipitable form. Mossbauer spectroscopy showed a gradual shift from intracellular iron particles less than 1.8 nm in diameter, through particles of intermediate size, to ferritin-like aggregates over 3.0 nm in diameter, reaching about 20% of total iron by 24 h. Ultrastructural studies showed premature damage such as mitochondrial abnormalities and excessive autophagocytosis. Small, 2.0-5.0 nm electron-dense cytosolic particles were noticed at 3 h of iron loading and reached maximal concentrations at 6 h. This was followed by accumulation of the small particles and of typical iron-rich ferritin cores within siderosomes. Because of the limited duration of iron loading and the high concentrations of non-transferrin inorganic iron employed, the present model is more relevant to acute than chronic iron overload. The efficient incorporation of large amounts of iron within ferritin molecules and its subsequent segregation, together with other smaller particles, within membrane-bound bodies, may represent a defence mechanism limiting iron toxicity in the face of advanced cytosiderosis.
UR - http://www.scopus.com/inward/record.url?scp=0023150822&partnerID=8YFLogxK
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C2 - 3814501
AN - SCOPUS:0023150822
SN - 0007-1021
VL - 68
SP - 53
EP - 65
JO - British Journal of Experimental Pathology
JF - British Journal of Experimental Pathology
IS - 1
ER -