International Journal of Cell Cloning, Vol 5, 122-133, Copyright © 1987 by AlphaMed Press
Lithium and hematopoietic toxicity. II. Acceleration in vivo of murine hematopoietic progenitor cells (CFU-gm and CFU-meg) following treatment with vinblastine sulfate
VS Gallicchio
Suppression of hematopoiesis is far too often the main consequence of
antineoplastic therapy, such that the developing degree of myelosuppression
and/or thrombocytopenia are usually the rate-limiting steps to adjuvant
therapy. This communication reports the results of studies designed to
investigate the capability of lithium to accelerate in vivo hematopoietic
recovery following exposure to vinblastine sulfate (VB). Male mice (144
BC3F1) received VB (4 mg/kg/b.w.) i.v. Twenty-four h following VB, 72 mice
received 35 micrograms m/animal, ultra-pure lithium carbonate (Li2CO3) i.p.
Another 72 mice received either VB or phosphate buffered saline as
controls. Beginning 24 h later and continuing on days 2, 5, 7, 9, 12, 21
and 28, three mice from each group were randomly sacrificed and their
hematological parameters analyzed. Bone marrow and splenic
granulocyte-macrophage progenitor cells (CFU-gm) and megakaryocyte
progenitor cells (CFU-meg) content were evaluated. Lithium was unable to
prevent the onset of either neutropenia or thrombocytopenia; however,
lithium was successful in restoring normal white blood cell and platelet
values earlier than the VB control group, thus significantly reducing the
period of drug- induced neutropenia and thrombocytopenia. This
lithium-enhanced hematopoiesis was measured by an accelerated recovery in
both marrow and splenic CFU-gm and CFU-meg compared to controls. These data
demonstrate the efficacy of lithium to accelerate hematopoietic recovery
following exposure to cytotoxic antineoplastic drugs.
