Hays E F, Margaretten N
Exp Hematol. 1985 Mar;13(3):229-34.
Marrow hypoplasia is described in CBA/H mice that drank water containing 300 mg/liter cadmium chloride for 12 months. This was characterized by a significant reduction of the totipotent stem cells (CFU-s), granulocyte-monocyte progenitor cells (GM-CFUc), and erythroid progenitor cells (CFU-e). The bone marrow cellularity and the proliferative capacity of GM-CFUc in vitro were decreased. The animals reflected these marrow alterations by demonstrating an anemia with reticulocytopenia and neutropenia. They did not show increased mortality or increased susceptibility to infections; however, their body weight was significantly reduced. In addition, iron deficiency was demonstrated in the cadmium-treated mice. The animals had a hypochromia of the peripheral red cells and diminished marrow iron stores. Thus, the anemia of cadmium toxicity is probably the combined result of bone marrow hypoplasia and iron deficiency.
在饮用含300毫克/升氯化镉的水达12个月的CBA/H小鼠中，观察到骨髓发育不全。其特征为全能干细胞（CFU-s）、粒细胞-单核细胞祖细胞（GM-CFUc）和红系祖细胞（CFU-e）显著减少。骨髓细胞数量以及GM-CFUc的体外增殖能力均降低。这些动物通过呈现伴有网织红细胞减少和中性粒细胞减少的贫血来反映这些骨髓改变。它们未表现出死亡率增加或对感染的易感性增加；然而，其体重显著减轻。此外，在经镉处理的小鼠中证实存在缺铁情况。这些动物外周红细胞出现低色素性，且骨髓铁储存减少。因此，镉中毒性贫血可能是骨髓发育不全和缺铁共同作用的结果。
