Manchester D K, Nicklas J A, O'Neill J P, Lippert M J, Grant S G, Langlois R G, Moore D H, Jensen R H, Albertini R J, Bigbee W L
Children's Hospital, Division of Genetic Services, Denver, CO 80218, USA.
Environ Mol Mutagen. 1995;26(3):203-12. doi: 10.1002/em.2850260304.
To assess the potential effect of maternal environments on human embryonic/fetal somatic mutation, we measured the frequencies of hypoxanthine-guanine phosphoribosyltransferase (HPRT, hprt gene), mutant T lymphocytes (Mf), and glycophorin A (GPA) variant erythrocytes (Vf) of both allele-loss (phi/N) and allele-loss-and-duplication (N/N) phenotypes in umbilical cord blood. The mean hprt Mf (1.40 +/- 1.11 x 10(-6), N = 66) and GPA Vf (phi/N 4.0 +/- 2.2 x 10(-6), N = 114; N/N 2.7 +/- 2.0 x 10(-6), N = 91) were significantly lower than those previously reported for adult populations. In addition, the hprt Mf was significantly higher than that of a published study of newborn cord blood samples from a geographically distant population (0.64 +/- 0.41 x 10(-6), N = 45, P < 0.01; t test, P < 0.01, Mann-Whitney U test). An examination of the demographic data from these two populations led to the sampling of 10 additional newborns specifically matched to the published study for maternal socioeconomic status. The hprt Mf (0.70 +/- 0.49 x 10(-6)) of this selected population was consistent with the published report and significantly lower than that of our initial population (P < 0.03, t test; P < 0.01, Mann-Whitney U test). These results indicate that there is an environmental effect related to maternal socioeconomic status on the frequency of embryonic/fetal somatic mutations. Molecular analyses of hprt mutants from this cohort with elevated Mf revealed a significant decrease in the relative contribution of gross structural mutations to the overall Mf (25 of 38, 66% vs. 34 of 41, 83%, P = 0.024, chi 2 test), suggesting that the higher Mf resulted from an elevated level of "point" mutations. No individual maternal demographic or environmental factor was identified as contributing more significantly than other any factor to the observed variability in hprt Mf or GPA Vf.
为评估母体环境对人类胚胎/胎儿体细胞突变的潜在影响,我们检测了脐带血中次黄嘌呤 - 鸟嘌呤磷酸核糖转移酶(HPRT,hprt基因)、突变型T淋巴细胞(Mf)以及糖蛋白A(GPA)变异红细胞(Vf)的频率,这些细胞具有等位基因缺失(phi/N)和等位基因缺失及重复(N/N)两种表型。hprt Mf的平均值(1.40±1.11×10⁻⁶,N = 66)以及GPA Vf的平均值(phi/N为4.0±2.2×10⁻⁶,N = 114;N/N为2.7±2.0×10⁻⁶,N = 91)显著低于先前报道的成年人群水平。此外,hprt Mf显著高于一项针对地理上遥远人群的新生儿脐带血样本的已发表研究结果(0.64±0.41×10⁻⁶,N = 45,P < 0.01;t检验,P < 0.01,曼 - 惠特尼U检验)。对这两个人群的人口统计学数据进行检查后,又额外选取了10名新生儿进行采样,这些新生儿在母体社会经济地位方面与已发表研究进行了专门匹配。该选定人群的hprt Mf(0.70±0.49×10⁻⁶)与已发表报告一致,且显著低于我们最初人群的水平(P < 0.03,t检验;P < 0.01,曼 - 惠特尼U检验)。这些结果表明,母体社会经济地位相关的环境因素对胚胎/胎儿体细胞突变频率存在影响。对该队列中Mf升高的hprt突变体进行分子分析发现,总体结构突变对总Mf的相对贡献显著降低(38个中有25个,66%对41个中有34个,83%,P = 0.024,卡方检验),这表明较高的Mf是由“点”突变水平升高导致的。未发现单个母体人口统计学或环境因素对观察到的hprt Mf或GPA Vf变异的贡献比其他任何因素更显著。