Recently I am researching about PRENATAL EXPOSURE; FETAL-GROWTH; CORD BLOOD; PERFLUOROALKYL SUBSTANCES; POLYCHLORINATED-BIPHENYLS; GENES; PBDES; SERUM; PCBS; AGE, Saw an article supported by the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health [HHSN275200800013C, HHSN275200800002I, HHSN27500006, HHSN275200800003IC, HHSN275200800014C, HHSN275200800012C, HHSN275200800028C, HHSN275201000009C, HHSN27500008, HHSN2752911999911]; National Institute on Minority Health and Health DisparitiesUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) – USANIH National Institute on Minority Health & Health Disparities (NIMHD); National Institute of Diabetes and Digestive and Kidney DiseasesUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) – USANIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK); NIH Office of the DirectorUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) – USA. Safety of Diphenyl oxide. Published in BMC in LONDON ,Authors: Ouidir, M; Mendola, P; Louis, GMB; Kannan, K; Zhang, CL; Tekola-Ayele, F. The CAS is 101-84-8. Through research, I have a further understanding and discovery of Diphenyl oxide
Background Prenatal maternal plasma persistent organic pollutant (POP) concentrations have been associated with neonatal outcomes. However, the underlying mechanisms remain unknown. Placental epigenetic mechanisms may be involved, but no prior epigenome-wide studies have investigated the impact of maternal POPs on placental DNA methylation. We studied the association between maternal plasma POP concentration in early pregnancy and epigenome-wide placental DNA methylation among 260 pregnant women from the NICHD Fetal Growth Studies. Results Our analysis focused on POPs with more than 80% plasma concentrations above the limit of quantification, including 3 organochlorine pesticides (hexachlorobenzene, trans-nonachlor,p,p’-dichlorodiphenyldichloroethylene), 1 polybrominated diphenyl ether (PBDE 47), 3 polychlorinated biphenyls (138/158, 153, 180), and 6 poly- and perfluorinated alkyl substances (PFASs) (perfluorodecanoic acid, perfluorohexanesulfonic acid, perfluorononanoic acid, perfluorooctanesulfonic acid, perfluoroundecanoic acid (PFUnDA)). Using 5% false discovery rate, POPs were associated with a total of 214 differentially methylated CpG sites (nominalpvalues ranging from 2.61 x 10(-21)to 2.11 x 10(-7)). Out of the 214 CpG sites, 24 (11%) were significantly correlated with placental expression of 21 genes. Notably, higher PFUnDA was associated with increased methylation at 3 CpG sites (cg13996963, cg12089439, cg18145877) annotated toTUSC3, and increased methylation at those 3 CpG sites was correlated with decreased expression ofTUSC3in the placenta. Increased methylation at cg18145877 (TUSC3) and decreased expression ofTUSC3were correlated with shorter birth length. Out of the 214 CpG sites, methylation at 44 CpG sites was correlated (pvalue < 0.10) with at least one neonatal anthropometry measure (i.e., birth weight, birth length, and head circumference). Seven CpG sites mediated (pvalue < 0.05) the association between PBDE 47 and neonatal anthropometry measures. Genes annotating the top differentially methylated CpG sites were enriched in pathways related to differentiation of embryonic cells (PBDE 47) and in pathways related to brain size and brain morphology (PFASs). Conclusions DNA methylation changes in the placenta were significantly associated with maternal plasma POPs concentration. The findings suggest that placental DNA methylation and gene expression mechanism may be involved in the prenatal toxicity of POPs and their association with neonatal anthropometry measures. Safety of Diphenyl oxide. Welcome to talk about 101-84-8, If you have any questions, you can contact Ouidir, M; Mendola, P; Louis, GMB; Kannan, K; Zhang, CL; Tekola-Ayele, F or send Email.
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