摘要
采用改良的g12细胞代替V79细胞,研究了六价铬[Cr(Ⅵ)]对gpt(xanthineguaninephosphoribosyltransferase,gpt,黄嘌呤鸟嘌呤磷酸核糖转移酶)位点的影响。结果表明,K2Cr2O7在引起细胞中毒不明显的低剂量0.625μmol/L(相当于铬含量64.99μg/L)即可诱发g12细胞gpt位点的突变,且高达本底的9倍以上;较高剂量组2.5μmol/L诱发的6-TG(6-thiogua-nine,6-巯基鸟嘌呤)突变体可达本底的50倍以上。K2Cr2O7诱发的g12细胞gpt位点突变在0~2.5μmol/L的K2Cr2O7范围内,具有明显的剂量-反应关系[y=24.27x-1.75,r=0.995,y为突变率(mutationrate),x为为K2Cr2O7剂量]。但随着K2Cr2O7的浓度增高,5.0μmol/L的K2Cr2O7组,由于细胞存活率太低,细胞数不够,达不到最后接种要求,不易继续进行。这一现象可能与K2Cr2O7的细胞毒性有关。因此,K2Cr2O7的遗传毒性及致突变性,只是在一定的剂量范围内遵循剂量反应规律。
The gpt locus of g12 cell is very sensitive to mutagens.In this paper,g12 cells were used to evaluate the mutagenicity of (K 2Cr 2O 7).Results revealed that 0 625μmol/L K 2Cr 2O 7 could induce the mutation of gpt locus,the mutation rate was about 8 fold higher than that of background.The mutation rate of gpt locus was dose dependent ( y =24 27 x -1 75, r =0 995, y :mutation rate; x :the dose of K 2Cr 2O 7) in the narrow range of 0—2 5μmol/L K 2Cr 2O 7.When above 2 5μmol/L K 2Cr 2O 7,the seeding efficiency was too low to do the further experiment because of the high cytotoxicity of K 2Cr 2O 7.In conclusion,K 2Cr 2O 7 could display high mutagenicity only in its narrow dose range. \ \
出处
《卫生毒理学杂志》
CSCD
1998年第2期71-73,共3页
Journal of Health Toxicology
基金
卫生部资助