Mitochondria, hemosomes and hemoglobin biosynthesis

Abstract

Erythroid cells of the liver and peripheral blood of rabbit embryos, as welt of bone-marrow and peripheral blood of adult rabbits with phenylhydrazine-induced hemolytic anemia, were analysed ultrastructurally to investigate the formation of hemosomes, organelles suggested to be sites of heme integration into the four globin polypeptides. After the incorporation of iron-containing material, free ferruginous inclusions appear. Mitochondria apparently give rise to lamellated bodies whose double lamellae expand for the captation of the ferruginous inclusions, a source of iron for heme synthesis, and globin polypeptidic chains already synthesized in the diffusely distributed polysomes. The expanding lamellae return, so that prehemosomal vesicles containing ferruginous material and globin are formed. Through invaginations of the inner membrane and a possible rotational movement of these vesicles the beginning of prohemosome formation takes place concomitant with the occurrence of heme synthesis. A structural rearrangement of prohemosomes occurs, and typical hemosomes containing hemoglobin molecules develop, whose content spreads throughout the cytoplasm by disruption of the organelle membranes.

Dynamics of mitochondria in living cells: Shape changes, dislocations, fusion, and fission of mitochondria

“…These differences may reflect different metabolic demands of the cytoplasm (Ord, 1979) or degenerative processes (e.g., Brunner et al, 1983;Kobolinsky and Beattie, 1977;Simon et al, 1969;Walker and Birt, 1969). The existence of differences in metabolic activities of mitochondria has been established in well spread cells in culture using membrane potential sensitive fluorochromes Smiley et al, 1991).…”

“…Mitochondria differing in matrix density, crista structure (i.e., coexistence of mitochondria with crestlike and with prismatic cristae) and density have been reported for a variety of cell types (e.g., Flickinger, 1968;Matile and Bahr, 1968;Ord and Smith, 1982). These differences may reflect different metabolic demands of the cytoplasm (Ord, 1979) or degenerative processes (e.g., Brunner et al, 1983;Kobolinsky and Beattie, 1977;Simon et al, 1969;Walker and Birt, 1969). The existence of differences in metabolic activities of mitochondria has been established in well spread cells in culture using membrane potential sensitive fluorochromes Smiley et al, 1991).…”