Hong H L, Silver M, Boorman G A
Chemical Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709.
Toxicology. 1988 Jun;50(1):107-15. doi: 10.1016/0300-483x(88)90125-4.
Ethylene glycol monomethyl ether (EGMME) has been reported to cause hematopoietic abnormalities in man. We have shown that mice exposed to EGMME post-natally have suppressed bone marrow cellularity and progenitor cells 8 weeks post-exposure which returns to normal values by 16 weeks. Studies were designed to determine whether EGMME exposed mice that recovered had evidence of residual marrow stem cell injury. B6C3F1 mice were injected subcutaneously with EGMME on days 1-5 after birth at doses of 0, 100, 200 and 400 mg/kg per day, allowed to recover, and stressed with 200 rads whole body irradiation at 15 and 21 weeks post-exposure. Bone marrow functions were examined during the recovery period. Mice that had been exposed to EGMME were more sensitive to irradiation and recovery of marrow cellularity and progenitor cell numbers occurred more slowly than in unexposed controls. This indicates that EGMME can cause persistent residual damage of bone marrow progenitor cells in mice, an effect that would not be apparent with routine hematological techniques.
据报道,乙二醇单甲醚(EGMME)可导致人类造血异常。我们已经表明,出生后接触EGMME的小鼠在接触后8周骨髓细胞数量和祖细胞受到抑制,到16周时恢复到正常水平。本研究旨在确定恢复后的EGMME暴露小鼠是否有残留骨髓干细胞损伤的证据。将B6C3F1小鼠在出生后第1至5天皮下注射EGMME,剂量为每天0、100、200和400 mg/kg,使其恢复,并在接触后15周和21周用200拉德全身照射进行应激处理。在恢复期检查骨髓功能。接触过EGMME的小鼠对辐射更敏感,骨髓细胞数量和祖细胞数量的恢复比未接触的对照组更慢。这表明EGMME可导致小鼠骨髓祖细胞持续的残留损伤,这种效应用常规血液学技术无法显现。