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Ultrastructure and cell cycle distribution of erythropoietic cells in heterozygotes and homozygotes for haemoglobin E
Author(s) -
Wickramasinghe S. N.,
Hughes Madeleine,
Wasi P.,
Fucharoen S.,
Litwinczuk R. A. C.
Publication year - 1984
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1984.tb02946.x
Subject(s) - erythroblast , heterozygote advantage , reticulocyte , biology , intracellular , globin , erythropoiesis , ineffective erythropoiesis , bone marrow , microbiology and biotechnology , cell cycle , cell , immunology , genetics , biochemistry , medicine , hemoglobin , genotype , rna , anemia , stem cell , haematopoiesis , gene
S ummary. Marrow aspirates from heterozygotes and homozygotes for haemoglobin E (HbE) have been studied by electron microscopy and by the technique of combined Feulgen microspectrophotometry and 3 H‐thymidine autoradiography. The erythropoietic cells of heterozygotes did not contain any precipitated globin chains and the proliferating erythroblasts of such individuals showed no abnormality in their distribution in the different stages of interphase. By contrast, 0–1.5% of late erythroblast profiles and 3.1–12.8% of marrow reticulocyte profiles of homozygotes contained intracellular inclusions resembling precipitated α‐chains. Although precipitated globin chains were not seen in the early polychromatic erythroblasts of homozygotes, the number of these cells in the G2 phase relative to that in the S phase was increased. These data indicate that there is (1) probably little or no imbalance of globin chain synthesis in heterozygotes, (2) a substantial degree of imbalance in homozygotes, and (3) a disturbance of erythroblast proliferation in homozygotes which cannot be attributed to the deleterious effects of detectable intracellular α‐chain precipitates. The electron microscope and cell cycle distribution data in the homozygotes for HbE were similar to those in two heterozygotes for β thalassaemia.