Caporossi D, Bacchetti S, Nicoletti B
Department of Public Health and Cellular Biology, II University of Rome, Italy.
Cancer Genet Cytogenet. 1991 Jul 1;54(1):39-53. doi: 10.1016/0165-4608(91)90028-s.
Infection of human embryonic kidney cells with adenoviruses results in the induction of gaps and breaks in cell chromosomes. With adenovirus type 12, cytogenetic damage is known to occur primarily at fragile sites on chromosomes 1 and 17. We have mapped adenovirus type 5-induced breaks and have observed that, although they occur on all chromosomes, they are localized primarily on bands where fragile sites have been mapped. The susceptibility of fragile sites to adenovirus led us to investigate their expression upon combined treatments with virus and aphidicolin, a frequently used inducer of fragile sites. Under these experimental conditions, the frequency of damage at all sites was found to increase significantly, and the magnitude of such increases indicated a synergistic effect between drug and virus.
腺病毒感染人胚肾细胞会导致细胞染色体出现间隙和断裂。已知12型腺病毒引起的细胞遗传学损伤主要发生在1号和17号染色体的脆性位点上。我们已绘制出5型腺病毒诱导的断裂图谱,并观察到,尽管这些断裂发生在所有染色体上,但它们主要定位在已绘制出脆性位点的条带处。脆性位点对腺病毒的易感性促使我们研究它们在病毒与阿非科林(一种常用的脆性位点诱导剂)联合处理后的表达情况。在这些实验条件下,发现所有位点的损伤频率显著增加,且这种增加的幅度表明药物与病毒之间存在协同效应。