HGPRT基因突变技术在检测化学诱变剂中的应用

本研究用Ｎ－甲基Ｎ＇－硝基亚硝基胍（ＭＮＮＧ）和苯并芘（Ｂ（ａ）Ｐ）诱导了中国仓鼠Ｖ７９细胞毒性和次黄嘌呤鸟嘌呤磷酸核糖基转移酶（ＨＧＰＲＴ）基因突变。结果表明，ＭＮＮＧ（０．７３５ｍｇ，Ｌ－１）和Ｂ（ａ）Ｐ（１ｍｇ·Ｌ－１）引起细胞存活率分别为７４．１％和７７．８％。阴性对照如空白对照、Ｓ９对照和溶剂对照的细胞自发突变频率低于０．４３×１０－５。ＭＮＮＧ和Ｂ（ａ）Ｐ＋Ｓ９诱发Ｖ７９细胞６－巯基鸟嘌呤抗性ＨＧＰＲＴ突变频率分别为１．１７×１０－５和１．３４×１０－５，比溶剂对照高４．９０和３．３５倍（Ｐ＜０．０１和Ｐ＜０．０５）。提示ＭＮＮＧ和Ｂ（ａ）Ｐ对Ｖ７９细胞呈细胞毒性和遗传毒性效应。

THE MUTATION TECHNIQUES AT THE HYPOXANTHINE-GUANINE PHOSPHORIBOSYL TRANSFERASE(HGPRT)GENE ARE APPLIED TO DETECIING CHEMICAL MUTAGENS

Cytotoxicity and mutation at the HGPRT gehe were induced by Nm-ethyl-N'-nitro-N-nitrosoguanidine(MNNG)and benzo(a)pyreneB(a)P] in V79 Chinese hamster cells.When the cells were treated with MNNG at the concentration of 0.735 mg·L-1 or B(a)P at 1.0mg·L-1,the cell survival efficiencies respectively were 74.1% or 77.8%. The spontaneous mutation frequercies of the negative controls,such as blank control, the rat liver microsome(S9)control and solvent control, were less than 0. 43 mutants per 105 cells in V79 cells. Both MNNG without S9 and B(a) P with S9 could induce 6-thioguanine resistance(6-TGr) mutation at the HGPRT gene,with the frequencies being 1. 17/105 cells and 1.34/105 cells,respectively. The mutation rates of MNNG and B(a)P+S9 separately were 4.90-fold and3.35-fold as large as those of solvent control(P<0.01 and P<0.05).The results imply that MNNG and B(a) P possess the cytotoxcity and hereditary toxicity in V79cells.