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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Castration decreases thrombocytopoiesis and testosterone restores platelet production in castrated BALB/c mice: evidence that testosterone acts on a bipotential hematopoietic precursor cell.

BALB/c male mice have higher platelet counts than female mice of the same strain. To test the hypothesis that testosterone influences platelet production, we evaluated indices of both red blood cell and platelet production in intact male BALB/c mice, in male mice 4 weeks after castration, and in castrated mice administered maintenance doses of testosterone as testosterone propionate. As predicted, castration resulted in decreased hematocrit and body weight in BALB/c mice. Body weights and hematocrits returned to noncastrated levels after 2 and 7 days, respectively, of administration of testosterone. Total circulating red blood cell mass and total circulating red blood cell count were both decreased by castration and were returned to control (noncastrated) levels after 2 days of testosterone therapy. Reticulocyte counts were not changed by castration, but they increased above counts of uncastrated and castrated control mice after 3 days of testosterone administration. White blood cell (WBC) numbers were unaffected by castration or testosterone administration. Additionally, platelet count (956 vs 834 x 10(3)/microliters), platelet size (3.87 vs 3.75 microns3), sulfur 35 incorporation into platelets (6.36 vs 4.87 x 10(-3)%), mean megakaryocyte ploidy (17.43N vs 16.89N), total circulating platelet mass (TCPM) (490 vs 379 x 10(8) microns3), and total circulating platelet count (TCPC) (131 vs 103 x 10(7)) were significantly (p < 0.05) decreased in castrated mice as compared with intact control mice.(ABSTRACT TRUNCATED AT 250 WORDS)[1]


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