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作 者:臧梦维
出 处:《皖南医学院学报》1996年第1期1-5,共5页Journal of Wannan Medical College
摘 要: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。Cytotoxicity and mutation at the HGPRT gehe were induced by Nm-ethyl-N'-nitro-N-nitrosoguanidine(MNNG)and benzo(a)pyrene[B(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.
分 类 号:R730.231.1[医药卫生—肿瘤]
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