Tucker A N, Hong L, Boorman G A, Luster M I
Thymus. 1986;8(3):121-7.
We have previously shown that the anticonvulsant drug, diphenylhydantoin (DPH), causes impaired humoral immunity and host resistance in subchronically treated mice as a consequence of myelotoxicity. The bone marrow is a primary and sensitive target for this drug, which causes a selective loss of stem cells in S phase. The present report describes the restoration of stem cell kinetics by thymosin in both drug-treated and folate-deficient mice. Thymosin and the thymic peptide, FTS (facteur thymique serique), were also able to protect the progenitor stem cell, CFU-GM, from DPH inhibition in vitro, indicating a direct effect of both drug and thymic factors on stem cells. Although the mechanism of this protection is not yet understood, the observation may have important implications concerning immunotherapy of DPH-treated epileptics, who are at increased risk of infectious diseases and malignancies.
我们先前已经表明，抗惊厥药物苯妥英（DPH）由于骨髓毒性，在亚慢性治疗的小鼠中会导致体液免疫和宿主抵抗力受损。骨髓是这种药物的主要且敏感的靶点，它会导致处于S期的干细胞选择性丢失。本报告描述了胸腺素在药物治疗和叶酸缺乏的小鼠中对干细胞动力学的恢复作用。胸腺素和胸腺肽FTS（血清胸腺因子）在体外也能够保护祖细胞CFU-GM免受DPH的抑制，表明药物和胸腺因子对干细胞都有直接作用。尽管这种保护机制尚不清楚，但这一观察结果可能对DPH治疗的癫痫患者的免疫治疗具有重要意义，这些患者患传染病和恶性肿瘤的风险增加。
