Golemboski K A, Sonnenfeld G
J Interferon Res. 1984 Summer;4(3):329-34. doi: 10.1089/jir.1984.4.329.
Embryonic fibroblasts were prepared from four different strains of mice: DBA/2, noninducible at the Ah locus for aryl hydrocarbon hydroxylase for carcinogen activation and, therefore, relatively resistant to tumor induction; C57BL/6, normal at the Ah locus; SENCAR, mice innately highly sensitive to tumor induction; and ICR, normal controls for SENCAR mice. The fibroblasts were exposed to the carcinogen benzo-(a)-pyrene at varying dosages. Alpha/beta IFN was next induced with poly(I)(C). Interferon production by cells from C57BL/6 mice was severely inhibited. Interferon production by DBA/2 cells was equally susceptible to inhibition by BP as IFN production by C57BL/6 cells, perhaps because of alternative pathways of activation of BP. Interferon production by SENCAR mouse cells was, on the other hand, much more susceptible to inhibition by BP than was IFN production by ICR mouse cells. These results suggest parallels between genetically controlled sensitivity to tumor induction by BP and genetically controlled susceptibility to inhibition of IFN induction by BP.
DBA/2，在芳烃羟化酶的Ah位点对致癌物激活无诱导性，因此对肿瘤诱导相对有抗性；C57BL/6，Ah位点正常；SENCAR，天生对肿瘤诱导高度敏感的小鼠；以及ICR，作为SENCAR小鼠的正常对照。将成纤维细胞暴露于不同剂量的致癌物苯并(a)芘中。接下来用聚肌苷酸:聚胞苷酸诱导α/β干扰素。C57BL/6小鼠细胞产生的干扰素受到严重抑制。DBA/2细胞产生的干扰素对苯并芘抑制的敏感性与C57BL/6细胞产生的干扰素相同，这可能是由于苯并芘的替代激活途径。另一方面，SENCAR小鼠细胞产生的干扰素比ICR小鼠细胞产生的干扰素对苯并芘抑制更敏感。这些结果表明，在对苯并芘诱导肿瘤的遗传控制敏感性与对苯并芘抑制干扰素诱导的遗传控制敏感性之间存在相似之处。
