粒细胞分化诱导小鼠模型中苯和苯二酚。

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榛子英航,奥康纳,Niculescu R, Kalf GF

粒细胞分化诱导小鼠模型中苯和苯二酚。

环境卫生教谕。1996年12月,104增刊6:1257 - 64。doi: 10.1289 / ehp.961041257。

PubMed ID

9118902 (在PubMed

]

文摘

人类长期接触苯引起急性髓系白血病(AML)。此处展示的研究以确定是否进行苯、或其活性代谢物,氢醌(HQ),影响成髓细胞的分化。苯或总部管理专门诱导C57BL / 6 j小鼠粒细胞分化成髓细胞。这些化合物的诱导分化的成髓细胞直接测试使用小鼠白介素3 (IL-3)端依赖32 d。3 (G)成髓细胞的细胞系,人类HL-60早幼粒细胞白血病细胞系。我们曾表明,苯治疗HL-60成髓细胞激活蛋白激酶C (PKC)和移植5-lipoxygenase(法律流程外包)的生产途径白三烯D4 (LTD4),一个重要的效应或粒细胞分化。分化被sphinganine阻止,PKC抑制剂,如下所示,通过法律外包抑制剂和LTD4受体拮抗剂。苯或总部也在32 d诱导分化。3 (G)成髓细胞。通常两个化合物与细胞信号通路激活粒细胞集落刺激因子(g - csf)和可以代替g - csf的要求。虽然IL-3 32 d诱导生长反应。3 (G)细胞,G - csf已被证明提供生长和分化的信号。 Both HQ and LTD4 induce differentiation and synergize with IL-3 for growth; however, neither supports growth in the absence of IL-3. Benzene, like HQ, also provides a differentiation signal for 32D cells; however, it has no effect on their growth. Unlike G-CSF, benzene, or LTD4, each of which stimulates terminal differentiation; HQ blocks differentiation at the myelocyte stage, allowing only a small percentage of progenitors to proceed to mature segmented granulocytes. Benzene- and G-CSF-induced differentiation were prevented by the additional of either LPO inhibitors or LTD4 receptor antagonists, indicating that benzene, like G-CSF, upregulates LTD4 production. Hydroquinone-induced differentiation was not affected by the LPO inhibitors, but only by the specific receptor antagonists. Thus HQ appears to obviate the requirement for LTD4 by activating the LTD4 receptor directly.

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药物靶点

药物	目标	类	生物	药理作用	行动
对苯二酚	半胱氨酰白三烯受体1	蛋白质	人类	未知的	激活剂	细节