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本文观察了一系列已知致癌物及其非致癌性类同物对经β—萘黄酮诱导过的或未经诱导的人FL细胞中的作用,以验证有ADPRT介导的,即可被ADPRT抑制剂防止的细胞NAD含量下降作为判断终点来检测化学物质诱发的DNA损伤的可能性。实验表明在MFO诱发过的FL细胞中AFB_1(1～100μmol/L),B(a)P(10～1000μmol/L),芘(1～1000μmol/L),DMA(10～100μmol/L),2—AAF(100～1000μmol/L)及 EC(10～1000μmol/L)可引起剂量依存性ADPRT介导的细胞NAD含量下降,而蒽(0.1～1000μmol/L),4—AAF(0.1～1000μmol/L),IsoPC(1～100μmol/L),黄樟素0.1～100μmol/L)及 Cy(1～100μmol/L)则否。直接作用致癌物ProLac(1～100μmol/L)及其非致癌性类同物BuLac(1～1000μmol/L)在MFO未经诱导的FL细胞中皆不能诱发ADPRT介导的细胞NAD含量降低。与非程序性DNA合成试验结果相对比,上述结果表明这一以ADPRT介导的细胞NAD含量下降作为判断终点的新检测法是一个检测化学诱变剂/致癌物特异而价廉的方法,其特异性与灵敏度与UDS试验相仿。
This article examines the role of a range of known carcinogens and their non-oncogenic analogs in β-naphthoflavone-induced or uninduced human FL cells to verify that ADPRT-mediated, ie, ADPRT- The decrease in cellular NAD levels prevented by the inhibitor serves as the end point to determine the likelihood of chemical-induced DNA damage. Experiments show that AFB_1 (1 ~ 100μmol / L), B (a) P (10 ~ 1000μmol / L), pyrene (1 ~ 1000μmol / L), DMA (10 ~ 100μmol / L) 2-AAF (100-1000 μmol / L) and EC (10-1000 μmol / L) could induce dose-dependent ADPRT-mediated decrease of NAD content in cells, but anthracycline (0.1-1000 μmol / L) / L), IsoPC (1-100μmol / L), safrole 0.1-100μmol / L) and Cy (1-100μmol / L). Direct-acting carcinogen ProLac (1 ~ 100μmol / L) and its non-oncogenic congeneric BuLac (1-1000μmol / L) failed to induce ADPRT-mediated decrease in NAD content in un-induced FLO cells. In contrast to the non-programmed DNA synthesis test results, the above results suggest that this new assay that uses ADPRT-mediated reduction of cell NAD content as the endpoint of the assay is a method that is specific and inexpensive to detect chemical mutagens / carcinogens and which Specificity and sensitivity are similar to the UDS test.