Ultrastructure and Morphometric Analysis of Hypertrophic Nucleoli in Non-Hodgkin’s Lymphoma and Phytohemagglutinin-Stimulated Lymphocytes

Abstract

The ultrastructure of hypertrophic nucleoli in large cells from each of 5 successive cases of non-Hodgkin’s lymphoma (regardless of predominant cell type) showed irregularly rounded or ovoid, mostly compact forms with few scattered light spaces. Occasional nucleolonemal forms were noted. Few ring forms or transitional forms between ring and compact or nucleolonemal types were present. Granular components occupied 78.5 ± 1.0% of the mean total area of 132 lymphoma large cell nucleoli of all configurations studied. Hypertrophic nucleoli in 27 phytohemagglutinin (PHA)-stimulated lymphocytes were predominantly nucleolonemal with 74.2 ± 10.6% granular composition. The qualitative and quantitative distribution of nucleolar granular moieties did not vary significantly between individual cases of lymphoma nor quantitatively between these and nucleoli in PHA-stimulated lymphocytes. These observations lend further credence to the suggestion of the lymphocyte as a common progenitor cell type for the large B and T cell of malignant lymphomas. Some functional similarity of their nucleoli and those of PHA-stimulated lymphocytes in their participation in ribonucleic acid synthesis is implied. Generally compact nucleoli of lymphomas in contrast to nucleolonemal forms of PHA-stimulated lymphocytes may be pathognomonic for large lymphocytic cells undergoing neoplasia.

Phototoxicity of protoporphyrin as related to its subcellular localization in mice livers after short-term feeding with griseofulvin

“…From electron-microscopic studies, evidence has been presented that protoporphyrin in griseofulvin-induced protoporphyria accumulates in a close relationship with the mitochondrial outer membrane (Matilla & Molland, 1974;Shapiro et al, 1980). In agreement with this, we found about 60% of protoporphyrin of the mitochondria associated with the outer membrane.…”

“…After 3 days administration of griseofulvin, the subcellular distribution of liver protoporphyrin paralleled that of the mitochondrial marker enzymes, with the greatest concentration (per mg of protein) in the mitochondrial fraction (Table 1). Ultrastructurally, early alterations in griseofulvin-induced murine protoporphyria and in human erythropoietic protoporphyria are swelling of the mitochondria followed at a later stage by the appearance of distorted and bizarrely shaped mitochondria with needle-like crystals of protoporphyrin (Matilla & Molland, 1974;Gschnait et al, 1975b;Cripps et al, 1977;Shapiro et al, 1980). The hepatocyte content of NADH also declines (Shapiro et al, 1980).…”

“…Ultrastructurally, early alterations in griseofulvin-induced murine protoporphyria and in human erythropoietic protoporphyria are swelling of the mitochondria followed at a later stage by the appearance of distorted and bizarrely shaped mitochondria with needle-like crystals of protoporphyrin (Matilla & Molland, 1974;Gschnait et al, 1975b;Cripps et al, 1977;Shapiro et al, 1980). The hepatocyte content of NADH also declines (Shapiro et al, 1980). Accumulation of protoporphyrin within, or adjacent to, the mitochondria is also to be expected from the localization of coproporphyrinogen oxidase to the inner membrane space (Elder & Evans, 1978), protoporphyrinogen oxidase associated with the mitochondrial inner membrane (Poulson, 1976) and ferrochelatase firmly bound within the inner membrane (Jones & Jones, 1969).…”