Vanhorick M, Moens W
Carcinogenesis. 1983 Nov;4(11):1459-63. doi: 10.1093/carcin/4.11.1459.
The exposure of SV40-transformed Chinese hamster cells (line CO60) to 50-150 micrograms/ml of monomeric acrylamide for 24 h resulted in a very weak induction of the amplification of the SV40 DNA inserts as measured by in situ hybridization with radioactive SV40 DNA as probe. The weak SV40 DNA amplification observed might result from a weak DNA-damaging activity as biologically illustrated by the capacity of high concentrations of acrylamide to irreversibly inhibit the DNA synthesis rate of CO60 cells. Moreover, acrylamide synergistically enhanced both the cytotoxicity and the induction of SV40 DNA synthesis by the carcinogens ethylmethane sulfonate, benzo[a]pyrene, mitomycin C, 4-nitroquinoline-1-oxide, 8-azaguanine and 5-fluorodeoxyuridine. Although a weak inducer of SV40 DNA amplification by itself, acrylamide potentiated the genotoxicity of a series of chemical carcinogens. This finding should be taken into consideration when assessing the risk of this widely used chemical.
将SV40转化的中国仓鼠细胞（CO60细胞系）暴露于浓度为50 - 150微克/毫升的单体丙烯酰胺中24小时，通过以放射性SV40 DNA为探针的原位杂交检测，结果显示SV40 DNA插入片段的扩增诱导作用非常微弱。观察到的微弱的SV40 DNA扩增可能是由于较弱的DNA损伤活性，高浓度丙烯酰胺能够不可逆地抑制CO60细胞的DNA合成速率，从生物学角度说明了这一点。此外，丙烯酰胺协同增强了致癌剂甲磺酸乙酯、苯并[a]芘、丝裂霉素C、4 - 硝基喹啉 - 1 - 氧化物、8 - 氮杂鸟嘌呤和5 - 氟脱氧尿苷的细胞毒性以及对SV40 DNA合成的诱导作用。尽管丙烯酰胺本身是SV40 DNA扩增的弱诱导剂，但它增强了一系列化学致癌物的遗传毒性。在评估这种广泛使用的化学物质的风险时，应考虑这一发现。
