Poirier V, James M R, Arlett C F, Lehmann A R
Carcinogenesis. 1985 Jun;6(6):837-41. doi: 10.1093/carcin/6.6.837.
The cell strain 46BR, derived from an immunodeficient individual, is hypersensitive to the lethal effects of DNA-damaging agents, and of 3-aminobenzamide (3AB), the latter being an inhibitor of the enzyme ADP-ribosyltransferase (ADPRT). This hypersensitivity is not found with the noninhibitory analogue, 3-aminobenzoate. The NAD content of 46BR cells is similar to that of fibroblasts from normal human donors, as is the decrease in NAD content following treatment with dimethylsulphate. Both the activity of ADP-ribosyltransferase and its inhibition by 3AB in permeabilized cells are similar in 46BR and in normal cell strains. High concentrations of 3AB interfere with purine metabolism in cultured cells. Again this effect is similar in 46BR and normal cells. Thus there is no apparent anomaly either in the activity of ADPRT or in the gross effects of 3AB in 46BR. The sensitivity to 3AB may be caused by a defect in a specific acceptor for the ADP-ribose synthesized by ADPRT, or in some as yet undiscovered action of the inhibitor.
细胞系46BR源自一名免疫缺陷个体，对DNA损伤剂的致死效应高度敏感，对3 - 氨基苯甲酰胺（3AB）也高度敏感，后者是ADP - 核糖基转移酶（ADPRT）的抑制剂。而在使用非抑制性类似物3 - 氨基苯甲酸时未发现这种高度敏感性。46BR细胞的NAD含量与正常人类供体的成纤维细胞相似，用硫酸二甲酯处理后NAD含量的降低情况也相似。在46BR细胞和正常细胞系中，通透细胞中ADP - 核糖基转移酶的活性及其被3AB抑制的情况均相似。高浓度的3AB会干扰培养细胞中的嘌呤代谢。同样，这种效应在46BR细胞和正常细胞中相似。因此，在46BR细胞中，ADPRT的活性或3AB的总体效应均无明显异常。对3AB的敏感性可能是由ADPRT合成的ADP - 核糖的特定受体缺陷引起的，或者是由该抑制剂尚未发现的某些作用导致的。
