Farris G M, Benjamin S A
Department of Pathology and Parasitology, College of Veterinary Medicine and Biological Sciences, Colorado State University 80523.
Am J Vet Res. 1993 Aug;54(8):1374-9.
The mechanism of estrogen-induced myelotoxicosis is unknown, although evidence indicates that estrogen does not directly damage the bone marrow granulocyte-macrophage progenitor cells and that the thymus is a probable mediator of the bone marrow suppression. Estrogen-induced production of a myelopoiesis-inhibitory factor by canine thymic stromal cells in vitro has been observed. Then, presence of a myelopoiesis-inhibitory factor in canine serum was investigated immediately after estrogen administration in vivo. Maximal reduction in colony-forming units-granulocyte/macrophage growth by sera from individual dogs varied. Individual dog sensitivity to estrogen-induced myelotoxicosis is seen clinically, and the cause is unknown. This serum factor could have a role in the eventual bone marrow hypoplasia seen in estrogen-treated dogs and is possibly the same factor produced by cultured thymic stromal cells exposed to estrogen.
雌激素诱导的骨髓中毒机制尚不清楚，尽管有证据表明雌激素不会直接损伤骨髓粒细胞-巨噬细胞祖细胞，且胸腺可能是骨髓抑制的介导者。体外实验已观察到雌激素可诱导犬胸腺基质细胞产生一种抑制骨髓生成的因子。随后，在体内给予雌激素后，立即对犬血清中是否存在骨髓生成抑制因子进行了研究。来自个别犬的血清对集落形成单位-粒细胞/巨噬细胞生长的最大抑制程度各不相同。临床上可观察到个别犬对雌激素诱导的骨髓中毒敏感，但其原因尚不清楚。这种血清因子可能在雌激素处理的犬最终出现的骨髓发育不全中起作用，并且可能与暴露于雌激素的培养胸腺基质细胞产生的因子相同。
