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口服苯并(a)芘的急性血液毒性:Ah位点的作用。

Acute hematotoxicity of oral benzo(a)pyrene: the role of the Ah locus.

作者信息

Anselstetter V, Heimpel H

出版信息

Acta Haematol. 1986;76(4):217-23. doi: 10.1159/000206059.

Abstract

Our results show a marked acute hematotoxicity of oral benzo(a)pyrene (BaP) in D2 mice as well as the extreme resistance of BDF1 individuals to bone marrow toxicity induced by oral BaP. Continued oral BaP produced severe bone marrow depression in D2 mice affecting all myelopoietic lineages, but produced only moderate bone marrow depression in BDF1 mice affecting erythropoiesis only. Pluripotent hematopoietic stem cells were almost completely destroyed in D2 individuals, but only reduced to approximately 40% in BDF1 individuals after 7 days of BaP. D2 mice were killed by 13 days of continued oral BaP, but BDF1 mice were still alive and in good condition even after 19 days of continued oral BaP. Analysis of the bone marrow and peripheral blood changes showed that severe toxic chemical bone marrow depression in D2 mice by continued oral BaP cannot serve as an experimental model system of acute aplastic anemia.

摘要

我们的研究结果显示,口服苯并(a)芘(BaP)对D2小鼠具有显著的急性血液毒性,而BDF1个体对口服BaP诱导的骨髓毒性具有极强的抵抗力。持续口服BaP会使D2小鼠出现严重的骨髓抑制,影响所有骨髓造血谱系,但在BDF1小鼠中仅产生中度骨髓抑制,且仅影响红细胞生成。多能造血干细胞在D2个体中几乎完全被破坏,但在BaP处理7天后,BDF1个体中的多能造血干细胞仅减少至约40%。持续口服BaP 13天后D2小鼠死亡,但即使持续口服BaP 19天,BDF1小鼠仍存活且状态良好。对骨髓和外周血变化的分析表明,持续口服BaP导致D2小鼠出现严重的毒性化学性骨髓抑制,不能作为急性再生障碍性贫血的实验模型系统。

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