Kiss C, Balázs M, Kéri-Fülöp I
Department of Pediatrics, Medical University of Debrecen, Hungary.
Leuk Res. 1990;14(3):221-5. doi: 10.1016/0145-2126(90)90129-w.
Lipid fluidity in the plasma membrane of leukemia cells was determined by measuring steady-state fluorescence polarization (P) of 1,6-diphenyl-1,3,5-hexatriene. In vitro dexamethasone treatment induced a dose-, time- and temperature-dependent and reversible increase in P values of primary leukemia cells and glucocorticoid-sensitive leukemia cell lines having specific glucocorticoid receptors. Membrane fluidity of glucocorticoid-resistant subclones with impaired specific dexamethasone binding capacity was not influenced by the drug. The results of this study suggest that dexamethasone modulates leukemia cell membrane fluidity via a classical glucocorticoid receptor dependent pathway.
通过测量1,6-二苯基-1,3,5-己三烯的稳态荧光偏振（P）来测定白血病细胞质膜中的脂质流动性。体外地塞米松处理可诱导原发性白血病细胞和具有特异性糖皮质激素受体的糖皮质激素敏感白血病细胞系的P值出现剂量、时间和温度依赖性的可逆增加。具有受损的特异性地塞米松结合能力的糖皮质激素抗性亚克隆的膜流动性不受该药物影响。本研究结果表明，地塞米松通过经典的糖皮质激素受体依赖性途径调节白血病细胞膜流动性。
