Medina Sebastian, Xu Huan, Wang Shu Chun, Lauer Fredine T, Liu Ke Jian, Burchiel Scott W
The University of New Mexico College of Pharmacy, Department of Pharmaceutical Sciences, Albuquerque, NM 87131, United States.
Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, 300020, China.
Toxicol Lett. 2017 May 5;273:106-111. doi: 10.1016/j.toxlet.2017.03.021. Epub 2017 Mar 27.
Epidemiological studies report an association between chronic arsenic (As) exposure and anemia in men, and women who are predisposed to anemia. The purpose of these studies was to determine whether a 60 d drinking water exposure of adult male C57BL/6J mice to 0, 100, and 500ppb arsenite (As) results in anemia due to alterations in erythroid progenitor cell development in the bone marrow. Exposure to 500ppb As for 60 d resulted in a reduction of mean corpuscular hemoglobin (MCH) levels, but did not significantly alter red blood cell (RBC) counts, hemoglobin (Hgb) levels, mean corpuscular Hgb concentrations (MCHC), or mean corpuscular volumes (MCV). Attenuation of burst-forming unit-erythroid (BFU-E) colony formation was observed in bone marrow cells of mice exposed to 500ppb As. The differentiation of late-stage bone marrow erythroblasts as defined by CD71 and Ter119 surface marker expression was reduced with the 500ppb As exposure. Mice exposed to 500ppb As also had elevated serum levels of erythropoietin (EPO). Collectively, these results show that exposure to low levels of As attenuate the development of early BFU-E cells and reduce the differentiation of late-stage erythroblasts. This suppression of bone marrow erythropoiesis may be a contributing factor to the mild hypochromic anemia observed in 500ppb As exposed mice.
流行病学研究报告称,长期接触砷(As)与男性及易患贫血症的女性的贫血之间存在关联。这些研究的目的是确定成年雄性C57BL/6J小鼠连续60天饮用含0、100和500 ppb亚砷酸盐(As)的水是否会因骨髓中红系祖细胞发育的改变而导致贫血。连续60天接触500 ppb的As会导致平均红细胞血红蛋白(MCH)水平降低,但不会显著改变红细胞(RBC)计数、血红蛋白(Hgb)水平、平均红细胞血红蛋白浓度(MCHC)或平均红细胞体积(MCV)。在接触500 ppb As的小鼠骨髓细胞中观察到爆式红细胞集落形成单位(BFU-E)集落形成减弱。随着500 ppb As暴露,由CD71和Ter119表面标志物表达定义的晚期骨髓成红细胞的分化减少。接触500 ppb As的小鼠血清促红细胞生成素(EPO)水平也升高。总体而言,这些结果表明,低水平的As暴露会减弱早期BFU-E细胞的发育并减少晚期成红细胞的分化。这种对骨髓红细胞生成的抑制可能是在接触500 ppb As的小鼠中观察到的轻度低色素性贫血的一个促成因素。