Walton D G, Acton A B, Stich H F
Mutat Res. 1984 Oct;129(1):129-36. doi: 10.1016/0027-5107(84)90131-3.
In mammalian cells it has previously been observed that low DNA-repair activity is correlated with high chromosome-aberration frequency. Since fish cells typically express comparatively low amounts of DNA repair, the chromosome aberration test holds potential as a sensitive fish genotoxicity assay. A comparison of in vitro DNA-repair activity showed HF greater than CHO greater than Ul-H = Ul-F following exposure to MNNG and 4NQO. Although peak chromosome-aberration frequency varied CHO greater than Ul-H greater than HF, at comparable mutagen concentrations the relationship was Ul-H greater than HF greater than CHO following 4NQO exposure and Ul-H greater than HF = CHO after MNNG exposure. Analyzing for chromosome aberrations at high mutagen concentrations was not possible due to mitotic inhibition/toxicity which varied according to the mutagen and cell line. Micronuclei frequency varied CHO greater than Ul-H greater than HF = Ul-F. In CHO and Ul-H, a 10-15-fold increase over controls compares with only a 2-3-fold increase for HF and Ul-F. These differences are likely related, in part, to the cell-division rate of each line and the coincident repair of the damaged DNA. Reasons for the lack of negative correlation between DNA repair and chromosomal damage in fish cells are discussed.
在哺乳动物细胞中,此前已观察到低DNA修复活性与高染色体畸变频率相关。由于鱼类细胞通常表达相对少量的DNA修复蛋白,染色体畸变试验有望成为一种灵敏的鱼类遗传毒性检测方法。体外DNA修复活性的比较显示,在暴露于MNNG和4NQO后,HF大于CHO大于Ul-H = Ul-F。尽管染色体畸变频率峰值的变化为CHO大于Ul-H大于HF,但在相当的诱变剂浓度下,4NQO暴露后关系为Ul-H大于HF大于CHO,MNNG暴露后为Ul-H大于HF = CHO。由于有丝分裂抑制/毒性因诱变剂和细胞系而异,在高诱变剂浓度下分析染色体畸变是不可能的。微核频率的变化为CHO大于Ul-H大于HF = Ul-F。在CHO和Ul-H中,与对照组相比增加了10 - 15倍,而HF和Ul-F仅增加了2 - 3倍。这些差异可能部分与每个细胞系的细胞分裂速率以及受损DNA的同时修复有关。本文讨论了鱼类细胞中DNA修复与染色体损伤缺乏负相关的原因。