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Mechanism of arsenic‐induced inhibition of erythropoiesis in mice
Author(s) -
Morse Bernard S.,
Conlan Maureen,
Giuliani Dennis G.,
Nussbaum Murray
Publication year - 1980
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830080305
Subject(s) - erythropoiesis , arsenic , arsenite , ineffective erythropoiesis , arsenic toxicity , arsenate , reticulocyte , toxicity , dna synthesis , sodium arsenite , erythropoietin , biology , bone marrow , chemistry , anemia , biochemistry , endocrinology , medicine , immunology , dna , messenger rna , organic chemistry , gene
Anemia accompanies arsenic intoxication in man. The present studies were undertaken to clarify further the effects of arsenic on erythropoiesis. A dose‐related inhibition of red cell 59 Fe incorporation and reticulocyte response was observed in normal mice treated with a single injection of arsenic. Arsenite was approximately two times as inhibitory as arsenate. The effects of arsenic on erythropoietin‐induced erythroid differentiation revealed a significant inhibitory effect on young, proliferating marrow nucleated erythroid precursor cells. More mature, nonproliferating nucleated erythroid cells were resistant to the toxic action of arsenic. A dose‐related inhibitory effect of arsenic on DNA synthesis was observed in fetal liver nucleated erythroid cells incubated with 3 H thymidine. Ineffective erythropoiesis as well as the megaloblastic morphology accompanying aberrant DNA synthesis – manifestations of arsenic toxicity in man – were not evident in the present studies.