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POSGRAD出生队列研究中产前砷暴露对新生儿和基因DNA甲基化的影响

Prenatal Arsenic Exposure on DNA Methylation of and Genes of Newborns from the POSGRAD Birth Cohort Study.

作者信息

Lerma-Treviño Carolina, Hernández-Cadena Leticia, Acosta-Montes Jorge Octavio, Hernández-Montes Georgina, Alvarado-Cruz Isabel, Romieu Isabelle, Barraza-Villarreal Albino

机构信息

Centro de Investigación en Nutrición y Salud, Instituto Nacional de Salud Pública, Cuernavaca 62100, Mexico.

Dirección de Salud Ambiental, Instituto Nacional de Salud Pública, Cuernavaca 62100, Mexico.

出版信息

Toxics. 2024 Jun 30;12(7):476. doi: 10.3390/toxics12070476.

DOI:10.3390/toxics12070476
PMID:39058128
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11280544/
Abstract

Exposure to arsenic (As) is a public health problem associated with cancer (skin and colon) and it has been reported that epigenetic changes may be a potential mechanism of As carcinogenesis. It is pertinent to evaluate this process in genes that have been associated with cancer, such as and Gestation and delivery data were obtained from the POSGRAD study. Exposure to As was measured in urine during pregnancy. Gene methylation was performed by sodium bisulfite sequencing; 26 CpG sites for the gene and 21 for were analyzed. These sites are located on the CpG islands near the start of transcription. Sociodemographic characteristics were obtained by a questionnaire. The statistical analysis was performed using multiple linear regression models adjusted for potential confounders. Newborns with an As exposure above 49.4 μg g showed a decrease of 0.21% on the methylation rate in the sites CpG15, CpG19, and CpG21 of the gene (adjusted ß = -0.21, -value = 0.02). No statistically significant association was found between prenatal exposure to As and methylation of the gene. Prenatal exposure to As was associated with decreased DNA methylation at the CpG15, CpG19, and CpG21 sites of the gene. These sites can provide information to elucidate epigenetic mechanisms associated with prenatal exposure to As and cancer.

摘要

接触砷(As)是一个与癌症(皮肤癌和结肠癌)相关的公共卫生问题,并且据报道,表观遗传变化可能是砷致癌的潜在机制。评估与癌症相关的基因(如[具体基因名称缺失]和[具体基因名称缺失])中的这一过程是有意义的。妊娠和分娩数据来自POSGRAD研究。在怀孕期间测量尿液中的砷暴露量。通过亚硫酸氢钠测序进行基因甲基化检测;分析了[具体基因名称缺失]基因的26个CpG位点和[具体基因名称缺失]基因的21个CpG位点。这些位点位于转录起始附近的CpG岛上。通过问卷调查获取社会人口学特征。使用针对潜在混杂因素进行调整的多元线性回归模型进行统计分析。砷暴露量高于49.4μg/g的新生儿在[具体基因名称缺失]基因的CpG15、CpG19和CpG21位点的甲基化率下降了0.21%(调整后的β=-0.21,P值=0.02)。未发现产前砷暴露与[具体基因名称缺失]基因甲基化之间存在统计学上的显著关联。产前砷暴露与[具体基因名称缺失]基因的CpG15、CpG19和CpG21位点的DNA甲基化降低有关。这些位点可为阐明与产前砷暴露和癌症相关的表观遗传机制提供信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5258/11280544/9ab37334b0ed/toxics-12-00476-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5258/11280544/53990c3dca2e/toxics-12-00476-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5258/11280544/355decc84ab4/toxics-12-00476-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5258/11280544/3b97e31f28dc/toxics-12-00476-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5258/11280544/665e90abf2b3/toxics-12-00476-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5258/11280544/9ab37334b0ed/toxics-12-00476-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5258/11280544/53990c3dca2e/toxics-12-00476-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5258/11280544/355decc84ab4/toxics-12-00476-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5258/11280544/3b97e31f28dc/toxics-12-00476-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5258/11280544/665e90abf2b3/toxics-12-00476-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5258/11280544/9ab37334b0ed/toxics-12-00476-g005.jpg

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