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首页> 外文期刊>Occupational and environmental medicine >Prenatal and concurrent exposure to halogenated organic compounds and gene expression of CYP17A1, CYP19A1, and oestrogen receptor alpha and beta genes.
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Prenatal and concurrent exposure to halogenated organic compounds and gene expression of CYP17A1, CYP19A1, and oestrogen receptor alpha and beta genes.

机译：产前和并发暴露于卤代有机化合物以及CYP17A1，CYP19A1和雌激素受体α和β基因的基因表达。

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OBJECTIVE: To determine whether prenatal exposure to dichlorodiphenyl ethylene (DDE) and polychlorinated biphenyls (PCBs) and concurrent exposure to DDE, PCBs and polybrominated diphenylethers (PBDEs) affect gene expression of aromatase (CYP19A1), 17-alpha-hydroxylase (CYP17A1), and oestrogen receptors alpha and beta (ESR 1 and ESR2). METHODS: Based on maternal PCB and DDE levels in the parent generation of the Michigan Fisheater Cohort determined between 1973 and 1991, individual prenatal exposures were estimated and have been published. In 2007, female adult offspring of this cohort were examined. Gene expression and concurrent lipid-adjusted exposures to DDE, PCBs and PBDEs were measured in blood and serum, respectively. Using mixed models and path analyses, gene-expression data were regressed on prenatal and concurrent exposures controlling for confounders. RESULTS: 139 daughters of Michigan fisheaters (65.3%) participated in the investigation. While prenatal PCB levels were statistically significantly associated with decreased expression of the aromatase and 17-alpha-hydroxylase genes, prenatal DDE levels were significantly related to increased gene expression of aromatase but not of 17-alpha-hydroxylase. The DDE association seems to be mediated by concurrent lipid-adjusted p,p'-DDE serum levels. Prenatal and concurrent exposure of both PCBs and DDE had comparable effects. No association was found for PBDEs or for the gene expression of ESR 1 and ESR2. CONCLUSIONS: A 40-year antecedent prenatal exposure and concurrent levels of PCBs and DDE are associated with the expression of aromatase and 17-alpha-hydroxylase genes. Prenatal exposures to organochlorines may instigate long-term alterations of gene expression. Mechanisms of prenatal induction of persistent gene-expression alterations are speculated to be epigenetic in nature.
机译：目的：确定产前暴露于二氯二苯乙烯（DDE）和多氯联苯（PCBs）以及同时暴露于DDE，PCBs和多溴联苯醚（PBDEs）是否会影响芳香化酶（CYP19A1），17-α-羟化酶（CYP17A1）的基因表达，和雌激素受体α和β（ESR 1和ESR2）。方法：根据在1973年至1991年之间确定的密歇根州食鱼者队列的母代中的母体PCB和DDE含量，估算并发表了各个产前暴露量。在2007年，检查了该队列的成年雌性后代。分别在血液和血清中测量基因表达和同时经脂质调节的DDE，PCBs和PBDEs暴露量。使用混合模型和路径分析，对控制混杂因素的产前和同时暴露的基因表达数据进行了回归。结果：密歇根州食鱼者的139个女儿（占65.3％）参加了调查。虽然产前PCB水平与芳香化酶和17-α-羟化酶基因表达的降低在统计学上显着相关，但是产前DDE水平与芳香化酶的基因表达增加显着相关，而与17-α-羟化酶的表达却没有显着相关。 DDE关联似乎是由同时进行的脂质调节的p，p'-DDE血清水平介导的。多氯联苯和DDE的产前和并发暴露具有可比的效果。 PBDEs或ESR 1和ESR2的基因表达均未发现关联。结论：产前40年的出生前暴露以及PCB和DDE的同时存在与芳香酶和17-α-羟化酶基因的表达有关。产前暴露于有机氯可能会引起基因表达的长期改变。据推测，产前持续性基因表达改变的诱导机制本质上是表观遗传的。

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