Asymmetric DNA methylation between sister chromatids of metaphase chromosomes in mouse embryos upon bisphenol A action

Паткин, Е. Л.; Грудинина, Н. А.; Sasina, L. K.; Noniashvili, E. M.; Pavlinova, L. I.; Сучкова, И. О.; Kustova, M.E.; Kolmakov, Nikolay N.; Truong, Tran Van; Sofronov, G. A.

doi:10.1016/j.reprotox.2017.08.017

Cited by 10 publications

(10 citation statements)

References 53 publications

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“…Research has shown that disrupted DNA methylation can be induced by synthetic nonsteroidal estrogen-diethylstilbestrol [32][33][34]. Ample studies suggest evidence of DNA methylation damage due to exposure to chromium, mercury, trichloroethylene, dichloroacetic and trichloroacetic acid, bisphenol A (BPA), and many other substances [35][36][37][38][39][40][41][42].…”

Section: Introductionmentioning

confidence: 99%

Environmental Epigenetics and Genome Flexibility: Focus on 5-Hydroxymethylcytosine

Efimova

Koltsova

Krapivin

et al. 2020

IJMS

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Convincing evidence accumulated over the last decades demonstrates the crucial role of epigenetic modifications for mammalian genome regulation and its flexibility. DNA methylation and demethylation is a key mechanism of genome programming and reprogramming. During ontogenesis, the DNA methylome undergoes both programmed changes and those induced by environmental and endogenous factors. The former enable accurate activation of developmental programs; the latter drive epigenetic responses to factors that directly or indirectly affect epigenetic biochemistry leading to alterations in genome regulation and mediating organism response to environmental transformations. Adverse environmental exposure can induce aberrant DNA methylation changes conducive to genetic dysfunction and, eventually, various pathologies. In recent years, evidence was derived that apart from 5-methylcytosine, the DNA methylation/demethylation cycle includes three other oxidative derivatives of cytosine—5-hydroxymethylcytosine (5hmC), 5-formylcytosine, and 5-carboxylcytosine. 5hmC is a predominantly stable form and serves as both an intermediate product of active DNA demethylation and an essential hallmark of epigenetic gene regulation. This makes 5hmC a potential contributor to epigenetically mediated responses to environmental factors. In this state-of-the-art review, we consolidate the latest findings on environmentally induced adverse effects on 5hmC patterns in mammalian genomes. Types of environmental exposure under consideration include hypnotic drugs and medicines (i.e., phenobarbital, diethylstilbestrol, cocaine, methamphetamine, ethanol, dimethyl sulfoxide), as well as anthropogenic pollutants (i.e., heavy metals, particulate air pollution, bisphenol A, hydroquinone, and pentachlorophenol metabolites). We put a special focus on the discussion of molecular mechanisms underlying environmentally induced alterations in DNA hydroxymethylation patterns and their impact on genetic dysfunction. We conclude that DNA hydroxymethylation is a sensitive biosensor for many harmful environmental factors each of which specifically targets 5hmC in different organs, cell types, and DNA sequences and induces its changes through a specific metabolic pathway. The associated transcriptional changes suggest that environmentally induced 5hmC alterations play a role in epigenetically mediated genome flexibility. We believe that knowledge accumulated in this review together with further studies will provide a solid basis for new approaches to epigenetic therapy and chemoprevention of environmentally induced epigenetic toxicity involving 5hmC patterns.

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Section: Introductionmentioning

confidence: 99%

Environmental Epigenetics and Genome Flexibility: Focus on 5-Hydroxymethylcytosine

Efimova

Koltsova

Krapivin

et al. 2020

IJMS

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“…Epigenetic differences between sister chromatids could result in different gene expression patterns in daughter cells (Lansdorp et al ., 2012). The number of asymmetric methylated sister chromatids (AMSC) is significantly decreased in mice exposed to BPA, with the number of infertile females mice increased (Patkin et al ., 2017). There is a linear relationship between AMSC and the number of infertile female mice.…”

Section: Dna Methylation and The Reproductive Toxicity Of Eedsmentioning

confidence: 99%

The role of epigenetics in the reproductive toxicity of environmental endocrine disruptors

Shi

et al. 2020

Environ and Mol Mutagen

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Environmental endocrine disruptors (EEDs) seriously endanger human health by interfering with the normal function of reproductive systems. In males, EEDs can affect sperm formation and semen quality as well spermatogenesis, ultimately reducing fertility. In females, EEDs can affect uterine development and the expression levels of reproduction-related genes, ultimately reducing female fertility and the normal development of the fetus. There are a large number of putative mechanisms by which EEDs can induce reproductive toxicity, and many studies have shown the involvement of epigenetics. In this review, we summarize the role of DNA methylation, noncoding RNAs, genomic imprinting, chromatin remodeling and histone modification in the reproductive toxicity of EEDs.

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“…Поскольку существуют данные, что белки эстрогенного пути влияют на эпигенетический статус генов-мишеней (как на уровне метилирования ДНК, так и белков хроматина), изменяя уровень их транскрипционной актив ности [75,76], можно предположить, что и воздействие БФА имеет аналогичные эпигенетические механизмы. До настоящего времени было опубликовано ограниченное количество работ по исследованию эпигенетических последствий воздействия БФА на развивающийся организм [77][78][79]. Полученные данные подтверждают, что этот ксеноэстроген действительно может вызывать изменения в статусе метилирования ДНК экспрессирующихся генов.…”

Section: механизмы действия бисфенола а как вещества разрушающего эндокринную системуunclassified

“…Тогда как у зародышей 9-го дня развития, то есть в период раннего органогенеза, наблюдалось небольшое повышение уровня полногеномного метилирования ДНК. В то же время уже на 12-й день эмбрионального развития было выявлено как гипометилирование, так и гиперметилирование ДНК в зависимости не только от части тела (типа ткани), но и от веса эмбрионов [77][78][79]. Полученные данные подтверждают, что доимплантационное развитие является высокочувствительным периодом к воздействию БФА.…”

Section: эпигенетические эффекты бисфенола а и экспрессия геновunclassified

Bisphenol a and human diseases. Mechanisms of action

Dergacheva

Паткин

Сучкова

et al. 2019

Ecological genetics

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Asymmetric DNA methylation between sister chromatids of metaphase chromosomes in mouse embryos upon bisphenol A action

Cited by 10 publications

References 53 publications

Environmental Epigenetics and Genome Flexibility: Focus on 5-Hydroxymethylcytosine

Environmental Epigenetics and Genome Flexibility: Focus on 5-Hydroxymethylcytosine

The role of epigenetics in the reproductive toxicity of environmental endocrine disruptors

Bisphenol a and human diseases. Mechanisms of action

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