In mice administered estradiol benzoate (EB) at 0.2 or 5 .mu.g dose levels, the number of erythroid colony-forming units (CFU-E) in marrow declines progressively starting from 12 through 48 h. Hypoxic erythropoietin (Ep) production, although potentiated in animals primed with relatively large dosages of EB (5-25 .mu.g), is significantly diminished after treatment with lower amounts of estrogen (0.2 .mu.g). In mice primed with large amounts of EB the enhancement of Ep activity apparently compensates the depleting influence on marrow CFU-E, leading to a near-normal erythroid response to hypoxia. A sharp drop of this parameter is observed in animals primed with the lower dosage (0.2 .mu.g), i.e., the depleting influence on the CFU-E pool is not compensated by potentiation of the Ep response.
ERYTHROID COLONY FORMATION AND ERYTHROPOIETIN ACTIVITY IN MICE TREATED WITH ESTRADIOL BENZOATE
MAGLI M C;
1977
Abstract
In mice administered estradiol benzoate (EB) at 0.2 or 5 .mu.g dose levels, the number of erythroid colony-forming units (CFU-E) in marrow declines progressively starting from 12 through 48 h. Hypoxic erythropoietin (Ep) production, although potentiated in animals primed with relatively large dosages of EB (5-25 .mu.g), is significantly diminished after treatment with lower amounts of estrogen (0.2 .mu.g). In mice primed with large amounts of EB the enhancement of Ep activity apparently compensates the depleting influence on marrow CFU-E, leading to a near-normal erythroid response to hypoxia. A sharp drop of this parameter is observed in animals primed with the lower dosage (0.2 .mu.g), i.e., the depleting influence on the CFU-E pool is not compensated by potentiation of the Ep response.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
