Epigenetic modifications associated with in utero exposure to endocrine disrupting chemicals BPA, DDT and Pb

Onuzulu, Chinonye Doris; Rotimi, Oluwakemi A.; Rotimi, Solomon O.

doi:10.1515/reveh-2018-0059

Cited by 33 publications

(27 citation statements)

References 154 publications

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“…The specific manifestations are: disruption of major weight control hormones such as catecholamine, thyroid hormone, estrogen, insulin, growth hormone, leptin, testosterone and corticosteroids; altered hormone sensitivity, especially for dopamine, serotonin, and angiotensin; and disruption of metabolic processes. Together, these effects can lead to tissue and organ damage, especially in nerves and muscles [12][13][14][15][16] , even at low levels of exposure. In our study, pregnant mice were administered DBP was from the 12th day of gestation to the 7th day after birth, a critical period in the differentiation of adipose tissue, reproductive organs and the immune system.…”

Section: Discussionmentioning

confidence: 99%

Intrauterine exposure to low-dose DBP in the mice induces obesity in offspring via suppression of UCP1 mediated ER stress

Li¹,

Li²,

Qu³

et al. 2020

Sci Rep

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Dibutyl phthalate (DBP) is recognized as an environmental endocrine disruptor that has been detected in fetal and postnatal samples. Recent evidence found that in utero DBP exposure was associated with an increase of adipose tissue weight and serum lipids in offspring, but the precise mechanism is unknown. Here we aimed to study the effects of in utero DBP exposure on obesity in offspring and examine possible mechanisms. SPF C57BL/6J pregnant mice were gavaged with either DBP (5 mg /kg/day) or corn oil, from gestational day 12 until postnatal day 7. After the offspring were weaned, the mice were fed a standard diet for 21 weeks, and in the last 2 weeks 20 mice were selected for TUDCA treatment. Intrauterine exposure to low-dose DBP promoted obesity in offspring, with evidence of glucose and lipid metabolic disorders and a decreased metabolic rate. Compared to controls, the DBP exposed mice had lower expression of UCP1 and significantly higher expression of Bip and Chop, known markers of endoplasmic reticulum (ER) stress. However, TUDCA treatment of DBP exposed mice returned these parameters nearly to the levels of the controls, with increased expression of UCP1, lower expression of Bip and Chop and ameliorated obesity. Intrauterine exposure of mice to low-dose DBP appears to promote obesity in offspring by inhibiting UCP1 via ER stress, a process that was largely reversed by treatment with TUDCA.

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Section: Discussionmentioning

confidence: 99%

Intrauterine exposure to low-dose DBP in the mice induces obesity in offspring via suppression of UCP1 mediated ER stress

Li¹,

Li²,

Qu³

et al. 2020

Sci Rep

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“…We also discovered that the urine BPA metabolite level was significantly higher in Taiwanese children than in those of other countries [9,10]. BPA has become serious public health problem globally and been described the various epigenetic mechanisms, like DNA methylation, histone modifications and non-coding RNAs, then affecting gene expression [11][12][13]. Furthermore, we found that exposure to this harmful chemical affected DNA methylation, which influenced the prevalence of allergic disorders in children [14].…”

Section: Introductionmentioning

confidence: 74%

Bisphenol a Exposure, DNA Methylation, and Asthma in Children

Yang

Karmaus

Yang³

et al. 2020

IJERPH

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Epidemiological studies have reported the relationship between bisphenol A (BPA) exposure and increased prevalence of asthma, but the mechanisms remain unclear. Here, we investigated whether BPA exposure and DNA methylation related to asthma in children. We collected urinary and blood samples from 228 children (Childhood Environment and Allergic Diseases Study cohort) aged 3 years. Thirty-three candidate genes potentially interacting with BPA exposure were selected from a toxicogenomics database. DNA methylation was measured in 22 blood samples with top-high and bottom-low exposures of BPA. Candidate genes with differential methylation levels were validated by qPCR and promoter associated CpG islands have been investigated. Correlations between the methylation percentage and BPA exposure and asthma were analyzed. According to our findings, MAPK1 showed differential methylation and was further investigated in 228 children. Adjusting for confounders, urinary BPA glucuronide (BPAG) level inversely correlated with MAPK1 promoter methylation (β = −0.539, p = 0.010). For the logistic regression analysis, MAPK1 methylation status was dichotomized into higher methylated and lower methylated groups with cut off continuous variable of median of promoter methylation percentage (50%) while performing the analysis. MAPK1 methylation was lower in children with asthma than in children without asthma (mean ± SD; 69.82 ± 5.88% vs. 79.82 ± 5.56%) (p = 0.001). Mediation analysis suggested that MAPK1 methylation acts as a mediation variable between BPA exposure and asthma. The mechanism of BPA exposure on childhood asthma might, therefore, be through the alteration of MAPK1 methylation. The mechanism of BPA exposure on childhood asthma might, therefore, be through the alteration of MAPK1 methylation.

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“…As discussed previously, the mammary gland goes through several developmental periods including prenatal, postnatal, and puberty. During this time, the mammary gland might be more sensitive to epigenetic modifications and disruptions [8,9].…”

Section: Epigenetic Modificationsmentioning

confidence: 99%

Epigenetics: New Insights into Mammary Gland Biology

Ivanova

Guillou

Hue-Beauvais

et al. 2021

Genes

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The mammary gland undergoes important anatomical and physiological changes from embryogenesis through puberty, pregnancy, lactation and involution. These steps are under the control of a complex network of molecular factors, in which epigenetic mechanisms play a role that is increasingly well described. Recently, studies investigating epigenetic modifications and their impacts on gene expression in the mammary gland have been performed at different physiological stages and in different mammary cell types. This has led to the establishment of a role for epigenetic marks in milk component biosynthesis. This review aims to summarize the available knowledge regarding the involvement of the four main molecular mechanisms in epigenetics: DNA methylation, histone modifications, polycomb protein activity and non-coding RNA functions.

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Epigenetic modifications associated with in utero exposure to endocrine disrupting chemicals BPA, DDT and Pb

Cited by 33 publications

References 154 publications

Intrauterine exposure to low-dose DBP in the mice induces obesity in offspring via suppression of UCP1 mediated ER stress

Intrauterine exposure to low-dose DBP in the mice induces obesity in offspring via suppression of UCP1 mediated ER stress

Bisphenol a Exposure, DNA Methylation, and Asthma in Children

Epigenetics: New Insights into Mammary Gland Biology

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