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Endocrinology Meets Environmental Epigenetics

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A special issue of International Journal of Environmental Research and Public Health (ISSN 1660-4601). This special issue belongs to the section "Toxicology and Public Health".

Deadline for manuscript submissions: closed (31 May 2021) | Viewed by 6853

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Special Issue Editor

Dr. Lavinia Casati

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Guest Editor

Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan 20129, Italy
Interests: epigenetics; histone modification; environment; nanoplastics; steroid receptor; oxidative stress; bone

Special Issue Information

Dear Colleagues,

Environmental epigenetics represents a new field of study of the epigenome. What is “environmental epigenetics”? Environmental epigenetics refers to how environmental exposure affects epigenetic changes. Twins share the same genome, but the environment changes their epigenome. The honey bee differentiates the workers from the queen through an epigenetic mechanism controlled by diet. Diet is one of the environmental modifiers of the epigenome (we are what our grandparents have eaten). What are the other modifiers? Lifestyle (e.g., alcohol consumption or smoking), oxidative stress, and environmental pollutants with particular attention to the endocrine disruptor compounds are involved in affecting the epigenome. EDCs mimic and disrupt the endocrine system; several pieces of evidence indicate the involvement of the epigenetic mechanism in EDCs’ disrupting actions. It is the first contact between environmental epigenetics and endocrinology. Nuclear receptors and, in particular, steroid receptors also act as cofactors of histone modifier enzymes, modulating the epigenome directly. Environmental epigenetics could mediate the effects of pollutants or nutrients with hormonal behavior (see genistein) and the development of endocrine diseases like diabetes type II or metabolic syndrome.

This Special Issue aims to make a new point of view about the role of the epigenetic mechanism affected by environmental cues that influence the endocrine system and the related diseases. Contributions, in the form of review, research papers, and case studies should be related to the following topics:

The relation between epigenetic mechanism and endocrine system (interplay between hormonal receptor and histone modifiers or DNA methylation and noncoding RNA);
The effects of the environment on epigenetics. Focus on (a) environmental pollutants (dioxins, BPA, pesticides, plasticizer, micro and nanoplastiscs, heavy metals), (b) diet (caloric restriction, high-fat diet, Mediterranean diet, or nutraceuticals like genistein, tocotrienols, green tea polyphenol ), and (c) oxidative stress.
Possible environmental influence in developing endocrine-related disease: involvement of the epigenetic mechanism. Focus on diseases like metabolic syndrome, diabetes, bone-related disease, endocrine-related cancer, and psychiatric disorder.

Dr. Lavinia Casati
Guest Editor

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Keywords

Epigenome, DNA methylation, histone modifications, noncoding RNA
Endocrine disruptor compounds (PCBs, dioxin, BPA, phthalates, pesticides, micro- and nanoplastics)
Diet (nutraceuticals, vitamin D, tocotrienols, genistein, polyphenols) and lifestyle (smoking)
Diabetes, metabolic syndrome, endocrine-related cancer, bone, psychiatric disorders

Published Papers (3 papers)

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Research

23 pages, 5032 KiB

Open AccessArticle

Sex Steroid Regulation of Oxidative Stress in Bone Cells: An In Vitro Study

by Valeria Sibilia, Daniele Bottai, Roberto Maggi, Francesca Pagani, Raffaella Chiaramonte, Domenica Giannandrea, Valentina Citro, Natalia Platonova and Lavinia Casati

Int. J. Environ. Res. Public Health 2021, 18(22), 12168; https://doi.org/10.3390/ijerph182212168 - 19 Nov 2021

Cited by 3 | Viewed by 1714

Abstract

Environmental stimuli, including sex hormones and oxidative stress (OS), affect bone balance, modifying the epigenetic profiles of key osteogenic genes. Nonetheless, the interplay between sex steroids, epigenome and OS has yet be fully elucidated. This paper aims to study in vitro the role of sex steroids in OS-induced alteration in bone cells’ homeostasis, and to assess the possible contribution of epigenetic modifications. Toward this purpose, osteoblast (MC3T3-E1) and osteocyte (MLOY-4) cell lines were exposed to two different sources of free oxygen radicals, i.e., tert-butyl hydroperoxide and dexamethasone, and the protective effect of pre-treatment with androgens and estrogens was evaluated. In particular, we analyzed parameters that reflect bone cell homeostasis such as cell viability, cell migration, transcriptomic profile, transcriptional activity, and epigenetic signature. Our findings indicate that estrogens and androgens counteract OS effects. Using partially overlapping strategies, they reduce OS outcomes regarding cell viability, cell migration, the transcriptomic profile of gene families involved in bone remodeling, and epigenetic profile, i.e., H3K4me3 level. Additionally, we demonstrated that the protective effect of steroids against OS on bone homeostasis is partially mediated by the Akt pathway. Overall, these results suggest that the hormonal milieu may influence the mechanisms of age-related bone disease. Full article

(This article belongs to the Special Issue Endocrinology Meets Environmental Epigenetics)

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15 pages, 1762 KiB

Open AccessArticle

Bone Marrow Oxidative Stress and Acquired Lineage-Specific Genotoxicity in Hematopoietic Stem/Progenitor Cells Exposed to 1,4-Benzoquinone

by Ramya Dewi Mathialagan, Zariyantey Abd Hamid, Qing Min Ng, Nor Fadilah Rajab, Salwati Shuib and Siti Razila Binti Abdul Razak

Int. J. Environ. Res. Public Health 2020, 17(16), 5865; https://doi.org/10.3390/ijerph17165865 - 13 Aug 2020

Cited by 15 | Viewed by 2491

Abstract

Hematopoietic stem/progenitor cells (HSPCs) are susceptible to benzene-induced genotoxicity. However, little is known about the mechanism of DNA damage response affecting lineage-committed progenitors for myeloid, erythroid, and lymphoid. Here, we investigated the genotoxicity of a benzene metabolite, 1,4-benzoquinone (1,4-BQ), in HSPCs using oxidative stress and lineage-directed approaches. Mouse bone marrow cells (BMCs) were exposed to 1,4-BQ (1.25–12 μM) for 24 h, followed by oxidative stress and genotoxicity assessments. Then, the genotoxicity of 1,4-BQ in lineage-committed progenitors was evaluated using colony forming cell assay following 7–14 days of culture. 1,4-BQ exposure causes significant decreases (p < 0.05) in glutathione level and superoxide dismutase activity, along with significant increases (p < 0.05) in levels of malondialdehyde and protein carbonyls. 1,4-BQ exposure induces DNA damage in BMCs by significantly (p < 0.05) increased percentages of DNA in tail at 7 and 12 μM and tail moment at 12 μM. We found crucial differences in genotoxic susceptibility based on percentages of DNA in tail between lineage-committed progenitors. Myeloid and pre-B lymphoid progenitors appeared to acquire significant DNA damage as compared with the control starting from a low concentration of 1,4-BQ exposure (2.5 µM). In contrast, the erythroid progenitor showed significant damage as compared with the control starting at 5 µM 1,4-BQ. Meanwhile, a significant (p < 0.05) increase in tail moment was only notable at 7 µM and 12 µM 1,4-BQ exposure for all progenitors. Benzene could mediate hematological disorders by promoting bone marrow oxidative stress and lineage-specific genotoxicity targeting HSPCs. Full article

(This article belongs to the Special Issue Endocrinology Meets Environmental Epigenetics)

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14 pages, 1736 KiB

Open AccessArticle

Maternal but Not Paternal High-Fat Diet (HFD) Exposure at Conception Predisposes for ‘Diabesity’ in Offspring Generations

by Karen Schellong, Kerstin Melchior, Thomas Ziska, Rebecca C. Rancourt, Wolfgang Henrich and Andreas Plagemann

Int. J. Environ. Res. Public Health 2020, 17(12), 4229; https://doi.org/10.3390/ijerph17124229 - 13 Jun 2020

Cited by 7 | Viewed by 2249

Abstract

While environmental epigenetics mainly focuses on xenobiotic endocrine disruptors, dietary composition might be one of the most important environmental exposures for epigenetic modifications, perhaps even for offspring generations. We performed a large-scale rat study on key phenotypic consequences from parental (F0) high-caloric, high-fat diet (HFD) food intake, precisely and specifically at mating/conception, focusing on ‘diabesity’ risk in first- (F1) and second- (F2) generation offspring of both sexes. F0 rats (maternal or paternal, respectively) received HFD overfeeding, starting six weeks prior to mating with normally fed control rats. The maternal side F1 offspring of both sexes developed a ‘diabesity’ predisposition throughout life (obesity, hyperleptinemia, hyperglycemia, insulin resistance), while no respective alterations occurred in the paternal side F1 offspring, neither in males nor in females. Mating the maternal side F1 females with control males under standard feeding conditions led, again, to a ‘diabesity’ predisposition in the F2 generation, which, however, was less pronounced than in the F1 generation. Our observations speak in favor of the critical impact of maternal but not paternal metabolism around the time frame of reproduction for offspring metabolic health over generations. Such fundamental phenotypic observations should be carefully considered in front of detailed molecular epigenetic approaches on eventual mechanisms. Full article

(This article belongs to the Special Issue Endocrinology Meets Environmental Epigenetics)

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