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首页> 外文期刊>Cancer epidemiology, biomarkers and prevention: A publication of the American Association for Cancer Research >Association between polycyclic aromatic hydrocarbon-DNA adduct levels in maternal and newborn white blood cells and glutathione S-transferase P1 and CYP1A1 polymorphisms.
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Association between polycyclic aromatic hydrocarbon-DNA adduct levels in maternal and newborn white blood cells and glutathione S-transferase P1 and CYP1A1 polymorphisms.

机译：孕妇和新生儿白细胞中多环芳烃-DNA加合物水平与谷胱甘肽S-转移酶P1和CYP1A1多态性之间的关联。

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摘要

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental pollutants; a number are carcinogenic. Metabolic polymorphisms may modulate susceptibility to PAH-induced DNA damage and carcinogenesis. This study investigates the relationship between PAH-DNA adduct levels (in maternal and newborn WBCs) and two polymorphisms: (a) an MspI RFLP in the 3' noncoding region of cytochrome P4501A1 (CYP1A1); and (b) an A-->G transition in nucleotide 313 of glutathione S-transferase P1 (GSTP1), resulting in an ile105val substitution. CYP1A1 catalyzes the bioactivation of PAH; the CYP1A1 MspI RFLP has been associated with cancer of the lung. GSTP1 catalyzes the detoxification of PAH; the val allele has greater catalytic efficiency toward PAH diol epoxides. The study involves 160 mothers and their newborns from Poland. Regression models controlled for maternal smoking and other confounders. No association was seen between maternal adduct levels and either polymorphism, separately or combined. However, adduct levels were higher among newborns with the CYP1A1 MspI restriction site (heterozygotes and homozygotes combined) compared with newborns lacking the restriction site (P = 0.06). Adducts were higher among GSTP1 ile/val and ile/ile newborns compared with GSTP1 val/val newborns (P = 0.08). Adduct levels were 4-fold higher among GSTP1 ile/ile newborns having the CYP1A1 restriction site compared with GSTP1 val/val newborns who lacked the CYP1A1 restriction site (P = 0.04). This study demonstrates a significant combined effect of phase I and phase II polymorphisms on DNA damage from PAHs in fetal tissues. It illustrates the importance of considering interindividual variation in assessing risks of transplacental exposure to PAHs.
机译：多环芳烃（PAHs）是普遍存在的环境污染物。一些是致癌的。代谢多态性可能会调节对PAH诱导的DNA损伤和致癌作用的敏感性。这项研究调查了PAH-DNA加合物水平（在母体和新生儿WBC中）与两个多态性之间的关系：（a）细胞色素P4501A1（CYP1A1）3'非编码区中的MspI RFLP。 （b）谷胱甘肽S-转移酶P1（GSTP1）核苷酸313的A→G过渡，导致ile105val取代。 CYP1A1催化PAH的生物活化。 CYP1A1 MspI RFLP与肺癌有关。 GSTP1催化PAH的解毒; val等位基因对PAH二醇环氧化物具有更高的催化效率。该研究涉及来自波兰的160名母亲及其新生儿。针对孕妇吸烟和其他混杂因素控制的回归模型。母体加合物水平与多态性（单独或联合）之间没有关联。然而，与没有限制位点的新生儿相比，具有CYP1A1 MspI限制位点的新生儿（杂合子和纯合子合并）的加合物水平更高（P = 0.06）。与GSTP1 val / val新生儿相比，GSTP1 ile / val和ile / ile新生儿的加合物更高（P = 0.08）。与没有CYP1A1限制性位点的GSTP1 val / val新生儿相比，具有CYP1A1限制性位点的GSTP1 ile / ile新生儿的加合物水平高4倍（P = 0.04）。这项研究表明，I和II期多态性对胎儿组织中PAHs造成的DNA损伤具有显着的综合作用。它说明了在评估胎盘暴露于PAHs的风险时考虑个体差异的重要性。

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