Depot iron, ferritin iron, and ferritin protein were measured in 34 liver needle biopsy specimens obtained from patients with primary and secondary iron-loading diseases.The patients were classified as idiopathic hemochromatosis (14), porphyria cutanea tarda (4), and iron-loading anemias (16). With accumulation of depot iron, the amount of liver ferritin protein increased, however, the ratio of ferritin protein to depot iron fell at concentrations of depot iron in excess of 1,000 pg per g m of liver. The liver ferritin protein concentration was not influenced by the specific kind of the iron storage disorder. The mean iron content of ferritin molecules increased about 50% in profound iron overload. In low grade iron overload, the bulk of depot iron was present as ferritin; however, in subjects with heavy iron overload, depot iron consisted of approximately equal amounts of hemosiderin (nonferritin iron) and ferritin iron.

Ferritin-like particles were observed in bile canaliculi of patients with iron overload. These particles have been further investigated by: a staining method enhancing the size and contrast of ferritin protein, and electron probe microanalysis detecting the presence of the elements iron and phosphorus. Morphological observation of coated vesicles in the cytoplasm adjacent to the bile canaliculi and coated pits in the canalicular membrane suggests a transport mechanism via membrane-bound organelles. Support is given to the theory that part of the iron, stored in the liver, leaves the hepatocyte by excretion of ferritin into the bile.

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