Fox R M, Kefford R F, Tripp E H, Taylor I W
Cancer Res. 1981 Dec;41(12 Pt 1):5141-50.
Cultured human T-cell leukemia lymphocytes have enhanced sensitivity to growth inhibition by deoxyadenosine. We have used flow cytometry to investigate the mechanism of deoxyadenosine toxicity in cultured T-leukemic cells. Comparative studies on deoxyadenosine-resistant Epstein-Barr virus-transformed B-lymphocyte cell lines were also performed. After exposure of T-cells to low concentrations of deoxyadenosine (3 microM), in the presence of an adenosine deaminase inhibitor (erythro-9-[3-(2-hydroxynonyl)]adenosine), accumulation of cells of cells with a G1 DNA content was demonstrated. In contrast, B-cell lines showed a similar degree of growth inhibition after exposure to 200 to 400 microM deoxyadenosine but were blocked in S phase. The T-cell G1 block was associated with a rise in the deoxyadenosine triphosphate pool, and both these phenomena were prevented by the addition of deoxycytidine. The biochemical mechanism of this G1 block induced by deoxyadenosine in T-cells is not understood.
培养的人T细胞白血病淋巴细胞对脱氧腺苷的生长抑制作用敏感性增强。我们利用流式细胞术研究了脱氧腺苷在培养的T白血病细胞中的毒性机制。还对耐脱氧腺苷的爱泼斯坦-巴尔病毒转化的B淋巴细胞系进行了比较研究。在腺苷脱氨酶抑制剂（erythro-9-[3-(2-羟基壬基)]腺苷）存在的情况下，将T细胞暴露于低浓度的脱氧腺苷（3 microM）后，证明了具有G1 DNA含量的细胞的积累。相比之下，B细胞系在暴露于200至400 microM脱氧腺苷后显示出相似程度的生长抑制，但被阻滞在S期。T细胞的G1期阻滞与三磷酸脱氧腺苷池的增加有关，并且通过添加脱氧胞苷可以防止这两种现象。脱氧腺苷在T细胞中诱导这种G1期阻滞的生化机制尚不清楚。
