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Advances in Endocrine Disruptors

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 43704

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Special Issue Editors

Prof. Dr. Nicolas Chevalier

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Guest Editor

Centre Hospitalier Universitaire de Nice, Hôpital de l'Archet, Service d'Endocrinologie, Diabétologie et Médecine de la Reproduction, Inserm U1065, 06000 Nice, France
Interests: endocrine disruptors; epidemiology; cancer; reproductive tract; endocrine disorders; thyroid; obesity
Special Issues, Collections and Topics in MDPI journals

Dr. Charlotte Hinault-Boyer

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Guest Editor

Centre Hospitalier Universitaire de Nice, Hôpital Pasteur, Laboratoire de Biochimie-Hormonologie, Inserm U1065, 06000 Nice, France
Interests: endocrine disruptors; adipose tissue; cancer; obesity; fetal programming; mass spectrometry; biochemistry
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Endocrine disruption is now considered a major health concern affecting all people worldwide. For the last few years, a large number of clinical and experimental studies have deepened and progressed our knowledge of the molecular mechanisms involved in endocrine disruption. Nevertheless, some issues still need to be documented: non-monotonic effects (low-dose effects), non-classical steroid receptors, new signaling pathways, the adverse effects of mixtures, transgenerational effects, and new screening tools. Furthermore, some data suggest that endocrine disruption is also observed with non-chemical factors (millimeter wave radiation, lightning cycles, chronic stress such as that observed during the recent lockdown, etc.) and affects new endocrine systems such as the parathyroid glands, adrenals, neurocognitive regulation, and taste regulation.

This Special Issue aims to review current advances in the field of endocrine disruption with the purpose of better understanding these unmet needs. Contributions to both animal models and/or humans, as well as to alternative tools, are encouraged, to shed light on the development of new hypotheses about endocrine disruption.

Prof. Dr. Nicolas Chevalier
Dr. Charlotte Hinault-Boyer
Guest Editors

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

Endocrine disruptor
Non-monotonic effects
Low-dose effects
Mixtures
Chemical agents
Physical agents
Non-classical receptors
Cancer
Reproductive tract
Thyroid
Adrenal
Parathyroid glands
Neurocognitive effects
Obesity
Diabetes
Metabolic disorders
Transgenerational effects
Epigenetics
Biomarkers
Screening tools

Published Papers (14 papers)

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Research

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15 pages, 2671 KiB

Open AccessArticle

The Endocrine Disruptor Compound Bisphenol-A (BPA) Regulates the Intra-Tumoral Immune Microenvironment and Increases Lung Metastasis in an Experimental Model of Breast Cancer

by Margarita Isabel Palacios-Arreola, Norma Angelica Moreno-Mendoza, Karen Elizabeth Nava-Castro, Mariana Segovia-Mendoza, Armando Perez-Torres, Claudia Angelica Garay-Canales and Jorge Morales-Montor

Int. J. Mol. Sci. 2022, 23(5), 2523; https://doi.org/10.3390/ijms23052523 - 25 Feb 2022

Cited by 8 | Viewed by 2642

Abstract

Breast cancer (BC) metastasis represents the main physiopathology leading to poor prognosis and death. Bisphenol A (BPA) is a pollutant, classified as an endocrine-disrupting chemical compound with estrogenic properties, their exposure in the early stages of neonatal life leads to an increase in the size and weight of breast tumors and induces cellular changes in the tumoral immune microenvironment where cytokines play a key role. Thus, we used female BALB/c mice exposed neonatally to a single dose of BPA. Once mice reached sexual maturity, a mammary tumor was induced, injecting 4T1 cells in situ. After 25 days of injection, we evaluated endocrine alterations, cytokine expression, tissue alterations denoted by macro or micro-metastasis in the lung, and cell infiltration induced by metastasis. We found that BPA neonatal treatment did not show significant endocrine alterations. Noteworthy, BPA led to an augmented rate of metastasis to the lung associated with higher intratumoral expression of IL-1β, IL-6, IFN-γ, TNF-α, and VEGF. Our data suggest that cytokines are key players in the induction of BC metastasis and that BPA (an environmental pollutant) should be considered as a risk factor in the clinical history of patients as a possible inductor of BC metastasis. Full article

(This article belongs to the Special Issue Advances in Endocrine Disruptors)

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14 pages, 3211 KiB

Open AccessArticle

The Enzymatic and Non-Enzymatic Antioxidant System Response of the Seagrass Cymodocea nodosa to Bisphenol-A Toxicity

by Paraskevi Malea, Danae Kokkinidi, Alkistis Kevrekidou and Ioannis-Dimosthenis S. Adamakis

Int. J. Mol. Sci. 2022, 23(3), 1348; https://doi.org/10.3390/ijms23031348 - 25 Jan 2022

Cited by 10 | Viewed by 2031

Abstract

The effects of environmentally relevant bisphenol A (BPA) concentrations (0.3, 1 and 3 μg L⁻¹) were tested at 2, 4, 6 and 8 days, on intermediate leaves, of the seagrass Cymodocea nodosa. Hydrogen peroxide (H₂O₂) production, lipid peroxidation, protein, phenolic content and antioxidant enzyme activities were investigated. Increased H₂O₂ formation was detected even at the lowest BPA treatments from the beginning of the experiment and both the enzymatic and non-enzymatic antioxidant defense mechanisms were activated upon application of BPA. Elevated H₂O₂ levels that were detected as a response to increasing BPA concentrations and incubation time, led to the decrease of protein content on the 4th day even at the two lower BPA concentrations, and to the increase of the lipid peroxidation at the highest concentration. However, on the 6th day of BPA exposure, protein content did not differ from the control, indicating the ability of both the enzymatic and non-enzymatic mechanisms (such as superoxide dismutase (SOD) and phenolics) to counteract the BPA-derived oxidative stress. The early response of the protein content determined that the Low Effect Concentration (LOEC) of BPA is 0.3 μg L⁻¹ and that the protein content meets the requirements to be considered as a possible early warning “biomarker” for C. nodosa against BPA toxicity. Full article

(This article belongs to the Special Issue Advances in Endocrine Disruptors)

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14 pages, 3086 KiB

Open AccessArticle

Bisphenol S Impairs Invasion and Proliferation of Extravillous Trophoblasts Cells by Interfering with Epidermal Growth Factor Receptor Signaling

by Elvis Ticiani, Yong Pu, Jeremy Gingrich and Almudena Veiga-Lopez

Int. J. Mol. Sci. 2022, 23(2), 671; https://doi.org/10.3390/ijms23020671 - 08 Jan 2022

Cited by 9 | Viewed by 1886

Abstract

The placenta supports fetal growth and is vulnerable to exogenous chemical exposures. We have previously demonstrated that exposure to the emerging chemical bisphenol S (BPS) can alter placental endocrine function. Mechanistically, we have demonstrated that BPS interferes with epidermal growth factor receptor (EGFR) signaling, reducing placenta cell fusion. Extravillous trophoblasts (EVTs), a placenta cell type that aids with vascular remodeling, require EGF to invade into the maternal endometrium. We hypothesized that BPS would impair EGF-mediated invasion and proliferation in EVTs. Using human EVTs (HTR-8/SVneo cells), we tested whether BPS could inhibit the EGF response by blocking EGFR activation. We also evaluated functional endpoints of EGFR signaling, including EGF endocytosis, cell invasion and proliferation, and endovascular differentiation. We demonstrated that BPS blocked EGF-induced phosphorylation of EGFR by acting as a competitive antagonist to EGFR. Transwell assay and a three-dimensional microfluidic chip invasion assay revealed that BPS exposure can block EGF-mediated cell invasion. BPS also blocked EGF-mediated proliferation and endovascular differentiation. In conclusion, BPS can prevent EGF-mediated EVT proliferation and invasion through EGFR antagonism. Given the role of EGFR in trophoblast proliferation and differentiation during placental development, our findings suggest that maternal exposure to BPS may contribute to placental dysfunction via EGFR-mediated mechanisms. Full article

(This article belongs to the Special Issue Advances in Endocrine Disruptors)

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17 pages, 1239 KiB

Open AccessArticle

Constitutively Activating Mutants of Equine LH/CGR Constitutively Induce Signal Transduction and Inactivating Mutations Impair Biological Activity and Cell-Surface Receptor Loss In Vitro

by Munkhzaya Byambaragchaa, Hoon-Ki Seong, Seung-Hee Choi, Dae-Jung Kim, Myung-Hwa Kang and Kwan-Sik Min

Int. J. Mol. Sci. 2021, 22(19), 10723; https://doi.org/10.3390/ijms221910723 - 03 Oct 2021

Cited by 8 | Viewed by 1606

Abstract

The signal transduction of the equine lutropin/choriogonadotropin receptor (eLH/CGR) is unclear in naturally occurring activating/inactivating mutants of this receptor, which plays an important role in reproductive physiology. We undertook the present study to determine whether conserved structurally related mutations in eLH/CGR exhibit similar mechanisms of signal transduction. We constructed four constitutively activating mutants (M398T, L457R, D564G, and D578Y) and three inactivating mutants (D405N, R464H, and Y546F); measured cyclic adenosine monophosphate (cAMP) accumulation via homogeneous time-resolved fluorescence assays in Chinese hamster ovary cells; and investigated cell-surface receptor loss using an enzyme-linked immunosorbent assay in human embryonic kidney 293 cells. The eLH/CGR-L457R-, -D564G-, and -D578Y-expressing cells exhibited 16.9-, 16.4-, and 11.2-fold increases in basal cAMP response, respectively. The eLH/CGR-D405N- and R464H-expressing cells presented a completely impaired signal transduction, whereas the Y546F-expressing cells exhibited a small increase in cAMP response. The cell-surface receptor loss was 1.4- to 2.4-fold greater in the activating-mutant-expressing cells than in wild-type eLH/CGR-expressing cells, but was completely impaired in the D405N- and Y546F-expressing cells, despite treatment with a high concentration of agonist. In summary, the state of activation of eLH/CGR influenced agonist-induced cell-surface receptor loss, which was directly related to the signal transduction of constitutively activating mutants. Full article

(This article belongs to the Special Issue Advances in Endocrine Disruptors)

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14 pages, 1421 KiB

Open AccessArticle

The Influence of Bisphenol A (BPA) on the Occurrence of Selected Active Substances in Neuregulin 1 (NRG1)-Positive Enteric Neurons in the Porcine Large Intestine

by Krystyna Makowska, Kamila Szymańska, Jarosław Całka and Sławomir Gonkowski

Int. J. Mol. Sci. 2021, 22(19), 10308; https://doi.org/10.3390/ijms221910308 - 24 Sep 2021

Cited by 3 | Viewed by 1441

Abstract

Bisphenol A (BPA) is a substance used in the manufacture of plastics which shows multidirectional adverse effects on living organisms. Since the main path of intoxication with BPA is via the gastrointestinal (GI) tract, the stomach and intestine are especially vulnerable to the impact of this substance. One of the main factors participating in the regulation of intestinal functions is the enteric nervous system (ENS), which is characterized by high neurochemical diversity. Neuregulin 1 (NRG1) is one of the lesser-known active substances in the ENS. During the present study (performed using the double immunofluorescence method), the co-localization of NRG1 with other neuronal substances in the ENS of the caecum and the ascending and descending colon has been investigated under physiological conditions and after the administration of BPA. The obtained results indicate that NRG1-positive neurons also contain substance P, vasoactive intestinal polypeptide, a neuronal isoform of nitric oxide synthase and galanin and the degree of each co-localization depend on the type of enteric plexus and the particular fragment of the intestine. Moreover, it has been shown that BPA generally increases the degree of co-localization of NRG1 with other substances. Full article

(This article belongs to the Special Issue Advances in Endocrine Disruptors)

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9 pages, 1396 KiB

Open AccessArticle

Quercetin Protects Human Thyroid Cells against Cadmium Toxicity

by Francesca Capriglione, Jessica Maiuolo, Marilena Celano, Giuseppe Damante, Diego Russo, Stefania Bulotta and Valentina Maggisano

Int. J. Mol. Sci. 2021, 22(13), 6849; https://doi.org/10.3390/ijms22136849 - 25 Jun 2021

Cited by 7 | Viewed by 2181

Abstract

Various natural compounds have been successfully tested for preventing or counteracting the toxic effects of exposure to heavy metals. In this study, we analyzed the effects of cadmium chloride (CdCl₂) on immortalized, non-tumorigenic thyroid cells Nthy-ori-3-1. We investigated the molecular mechanism underlying its toxic action as well as the potential protective effect of quercetin against CdCl₂-induced damage. CdCl₂ suppressed cell growth in a dose- and time-dependent manner (IC50 value ~10 μM) associated with a decrease in levels of phospho-ERK. In addition, CdCl₂ elicited an increase in reactive oxygen species (ROS) production and lipid peroxidation. A significant increase in GRP78, an endoplasmic reticulum (ER) stress-related protein, was also observed. Supplementation of quercetin counteracted the growth-inhibiting action of CdCl₂ by recovering ERK protein phosphorylation levels, attenuating ROS overproduction, decreasing MDA content and reducing the expression of GRP78 in cells exposed to CdCl₂. Thus, in addition to revealing the molecular effects involved in cadmium-induced toxicity, the present study demonstrated, for the first time, a protective effect of quercetin against cadmium-induced damages to normal thyroid cells. Full article

(This article belongs to the Special Issue Advances in Endocrine Disruptors)

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Review

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23 pages, 1054 KiB

Open AccessReview

Impact of Endocrine Disruptors upon Non-Genetic Inheritance

by Debbie Montjean, Anne-Sophie Neyroud, Marina G. Yefimova, Moncef Benkhalifa, Rosalie Cabry and Célia Ravel

Int. J. Mol. Sci. 2022, 23(6), 3350; https://doi.org/10.3390/ijms23063350 - 20 Mar 2022

Cited by 21 | Viewed by 3601

Abstract

Similar to environmental factors, EDCs (endocrine-disrupting chemicals) can influence gene expression without modifying the DNA sequence. It is commonly accepted that the transgenerational inheritance of parentally acquired traits is conveyed by epigenetic alterations also known as “epimutations”. DNA methylation, acetylation, histone modification, RNA-mediated effects and extracellular vesicle effects are the mechanisms that have been described so far to be responsible for these epimutations. They may lead to the transgenerational inheritance of diverse phenotypes in the progeny when they occur in the germ cells of an affected individual. While EDC-induced health effects have dramatically increased over the past decade, limited effects on sperm epigenetics have been described. However, there has been a gain of interest in this issue in recent years. The gametes (sperm and oocyte) represent targets for EDCs and thus a route for environmentally induced changes over several generations. This review aims at providing an overview of the epigenetic mechanisms that might be implicated in this transgenerational inheritance. Full article

(This article belongs to the Special Issue Advances in Endocrine Disruptors)

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30 pages, 1490 KiB

Open AccessReview

The Potent Phytoestrogen 8-Prenylnaringenin: A Friend or a Foe?

by Raimo Pohjanvirta and Atefeh Nasri

Int. J. Mol. Sci. 2022, 23(6), 3168; https://doi.org/10.3390/ijms23063168 - 15 Mar 2022

Cited by 11 | Viewed by 4242

Abstract

8-prenylnaringenin (8-PN) is a prenylated flavonoid, occurring, in particular, in hop, but also in other plants. It has proven to be one of the most potent phytoestrogens in vitro known to date, and in the past 20 years, research has unveiled new effects triggered by it in biological systems. These findings have aroused the hopes, expectations, and enthusiasm of a “wonder-drug” for a host of human diseases. However, the majority of 8-PN effects require such high concentrations that they cannot be reached by normal dietary exposure, only pharmacologically; thus, adverse impacts may also emerge. Here, we provide a comprehensive and up-to-date review on this fascinating compound, with special reference to the range of beneficial and untoward health consequences that may ensue from exposure to it. Full article

(This article belongs to the Special Issue Advances in Endocrine Disruptors)

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17 pages, 866 KiB

Open AccessReview

How to Differentiate General Toxicity-Related Endocrine Effects from Endocrine Disruption: Systematic Review of Carbon Disulfide Data

by Nathalie Printemps, Brigitte Le Magueresse-Battistoni, Sakina Mhaouty-Kodja, Catherine Viguié and Cécile Michel

Int. J. Mol. Sci. 2022, 23(6), 3153; https://doi.org/10.3390/ijms23063153 - 15 Mar 2022

Cited by 7 | Viewed by 2224

Abstract

This review provides an overview of the assessment of the endocrine disrupting (ED) properties of carbon disulfide (CS₂), following the methodology used at the European level to identify endocrine disruptors. Relevant in vitro, in vivo studies and human data are analyzed. The assessment presented here focuses on one endocrine activity, i.e., thyroid disruption, and two main adverse effects, neurotoxicity and cardiotoxicity. The data available on the different ED or non-ED modes of action (MoA), known to trigger these adverse effects, are described and the strength of evidence of the different MoA is weighted. We conclude that the adverse effects could be due to systemic toxicity rather than endocrine-mediated toxicity. This assessment illustrates the scientific and regulatory challenges in differentiating a specific endocrine disruption from an indirect endocrine effect resulting from a non-ED mediated systemic toxicity. This issue of evaluating the ED properties of highly toxic and reactive substances has been insufficiently developed by European guidance so far and needs to be further addressed. Finally, this example also raises questions about the capacity of the technics available in toxicology to address such a complex issue with certainty. Full article

(This article belongs to the Special Issue Advances in Endocrine Disruptors)

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25 pages, 1225 KiB

Open AccessReview

Bisphenol A (BPA) Leading to Obesity and Cardiovascular Complications: A Compilation of Current In Vivo Study

by Ruth Naomi, Muhammad Dain Yazid, Hasnah Bahari, Yong Yoke Keong, Retnagowri Rajandram, Hashim Embong, Soo Huat Teoh, Shariff Halim and Fezah Othman

Int. J. Mol. Sci. 2022, 23(6), 2969; https://doi.org/10.3390/ijms23062969 - 09 Mar 2022

Cited by 30 | Viewed by 6011

Abstract

BPA is one of the most common endocrine disruptors that is widely being manufactured daily nationwide. Although scientific evidence supports claims of negative effects of BPA on humans, there is also evidence suggesting that a low level of BPA is safe. However, numerous in vivo trials contraindicate with this claim and there is a high possibility of BPA exposure could lead to obesity. It has been speculated that this does not stop with the exposed subjects only, but may also cause transgenerational effects. Direct disruption of endocrine regulation, neuroimmune and signaling pathways, as well as gut microbiata, has been identified to be interrupted by BPA exposure, leading to overweight or obesity. In these instances, cardiovascular complications are one of the primary notable clinical signs. In regard to this claim, this review paper discusses the role of BPA on obesity in the perspective of endocrine disruptions and possible cardiovascular complications that may arise due to BPA. Thus, the aim of this review is to outline the changes in gut microbiota and neuroimmune or signaling mechanisms involved in obesity in relation to BPA. To identify potentially relevant articles, a depth search was done on the databases Nature, PubMed, Wiley Online Library, and Medline & Ovid from the past 5 years. According to Boolean operator guideline, selected keywords such as (1) BPA OR environmental chemical AND fat OR LDL OR obese AND transgenerational effects or phenocopy (2) Endocrine disruptors OR chemical AND lipodystrophy AND phenocopy (3) Lipid profile OR weight changes AND cardiovascular effect (4) BPA AND neuroimmune OR gene signaling, were used as search terms. Upon screening, 11 articles were finalized to be further reviewed and data extraction tables containing information on (1) the type of animal model (2) duration and dosage of BPA exposure (3) changes in the lipid profile or weight (4) genes, signaling mechanism, or any neuroimmune signal involved, and (5) transgenerational effects were created. In toto, the study indicates there are high chances of BPA exposure affecting lipid profile and gene associated with lipolysis, leading to obesity. Therefore, this scoping review recapitulates the possible effects of BPA that may lead to obesity with the evidence of current in vivo trials. The biomarkers, safety concerns, recommended dosage, and the impact of COVID-19 on BPA are also briefly described. Full article

(This article belongs to the Special Issue Advances in Endocrine Disruptors)

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19 pages, 379 KiB

Open AccessReview

Does Bisphenol A Confer Risk of Neurodevelopmental Disorders? What We Have Learned from Developmental Neurotoxicity Studies in Animal Models

by Chloe Welch and Kimberly Mulligan

Int. J. Mol. Sci. 2022, 23(5), 2894; https://doi.org/10.3390/ijms23052894 - 07 Mar 2022

Cited by 18 | Viewed by 4225

Abstract

Substantial evidence indicates that bisphenol A (BPA), a ubiquitous environmental chemical used in the synthesis of polycarbonate plastics and epoxy resins, can impair brain development. Clinical and epidemiological studies exploring potential connections between BPA and neurodevelopmental disorders in humans have repeatedly identified correlations between early BPA exposure and developmental disorders, such as attention deficit/hyperactivity disorder and autism spectrum disorder. Investigations using invertebrate and vertebrate animal models have revealed that developmental exposure to BPA can impair multiple aspects of neuronal development, including neural stem cell proliferation and differentiation, synapse formation, and synaptic plasticity—neuronal phenotypes that are thought to underpin the fundamental changes in behavior-associated neurodevelopmental disorders. Consistent with neuronal phenotypes caused by BPA, behavioral analyses of BPA-treated animals have shown significant impacts on behavioral endophenotypes related to neurodevelopmental disorders, including altered locomotor activity, learning and memory deficits, and anxiety-like behavior. To contextualize the correlations between BPA and neurodevelopmental disorders in humans, this review summarizes the current literature on the developmental neurotoxicity of BPA in laboratory animals with an emphasis on neuronal phenotypes, molecular mechanisms, and behavioral outcomes. The collective works described here predominantly support the notion that gestational exposure to BPA should be regarded as a risk factor for neurodevelopmental disorders. Full article

(This article belongs to the Special Issue Advances in Endocrine Disruptors)

22 pages, 781 KiB

Open AccessReview

Behavioral Effects of Exposure to Phthalates in Female Rodents: Evidence for Endocrine Disruption?

by Nolwenn Adam and Sakina Mhaouty-Kodja

Int. J. Mol. Sci. 2022, 23(5), 2559; https://doi.org/10.3390/ijms23052559 - 25 Feb 2022

Cited by 7 | Viewed by 2356

Abstract

Phthalates have been widely studied for their reprotoxic effects in male rodents and in particular on testosterone production, for which reference doses were established. The female rodent brain can also represent a target for exposure to these environmental endocrine disruptors. Indeed, a large range of behaviors including reproductive behaviors, mood-related behaviors, and learning and memory are regulated by sex steroid hormones. Here we review the experimental studies addressing the effects and mechanisms of phthalate exposure on these behaviors in female rodents, paying particular attention to the experimental conditions (period of exposure, doses, estrous stage of analyses etc.). The objective of this review is to provide a clear picture of the consistent effects that can occur in female rodents and the gaps that still need to be filled in terms of effects and mode(s) of action for a better risk assessment for human health. Full article

(This article belongs to the Special Issue Advances in Endocrine Disruptors)

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14 pages, 800 KiB

Open AccessReview

Endocrine-Disrupting Chemicals and Their Adverse Effects on the Endoplasmic Reticulum

by Kangmin Kim, Jin-Sook Kwon, Changhwan Ahn and Eui-Bae Jeung

Int. J. Mol. Sci. 2022, 23(3), 1581; https://doi.org/10.3390/ijms23031581 - 29 Jan 2022

Cited by 9 | Viewed by 3148

Abstract

There is growing concern regarding the health and safety issues of endocrine-disrupting chemicals (EDCs). Long-term exposure to EDCs has serious adverse health effects through both hormone-direct and hormone-indirect ways. Accordingly, some EDCs can be a pathogen and an inducer to the susceptibility of disease, even if they have a very low affinity on the estrogen receptor, or no estrogenic effect. Endoplasmic reticulum (ER) stress recently attracted attention in this research area. Because ER and ER stress could be key regulators of the EDC’s adverse effects, such as the malfunction of the organ, as well as the death, apoptosis, and proliferation of a cell. In this review, we focused on finding evidence which shows that EDCs could be a trigger for ER stress and provide specific examples of EDCs, which are known to cause ER stress currently. Full article

(This article belongs to the Special Issue Advances in Endocrine Disruptors)

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17 pages, 1033 KiB

Open AccessReview

Endocrine Disruptors and Prostate Cancer

by Margherita Corti, Stefano Lorenzetti, Alessandro Ubaldi, Romano Zilli and Daniele Marcoccia

Int. J. Mol. Sci. 2022, 23(3), 1216; https://doi.org/10.3390/ijms23031216 - 21 Jan 2022

Cited by 18 | Viewed by 3805

Abstract

The role of endocrine disruptors (EDs) in the human prostate gland is an overlooked issue even though the prostate is essential for male fertility. From experimental models, it is known that EDs can influence several molecular mechanisms involved in prostate homeostasis and diseases, including prostate cancer (PCa), one of the most common cancers in the male, whose onset and progression is characterized by the deregulation of several cellular pathways including androgen receptor (AR) signaling. The prostate gland essentiality relies on its function to produce and secrete the prostatic fluid, a component of the seminal fluid, needed to keep alive and functional sperms upon ejaculation. In physiological condition, in the prostate epithelium the more-active androgen, the 5α-dihydrotestosterone (DHT), formed from testosterone (T) by the 5α-reductase enzyme (SRD5A), binds to AR and, upon homodimerization and nuclear translocation, recognizes the promoter of target genes modulating them. In pathological conditions, AR mutations and/or less specific AR binding by ligands modulate differently targeted genes leading to an altered regulation of cell proliferation and triggering PCa onset and development. EDs acting on the AR-dependent signaling within the prostate gland can contribute to the PCa onset and to exacerbating its development. Full article

(This article belongs to the Special Issue Advances in Endocrine Disruptors)

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