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Progress in Research on Endocrine-Disrupting Chemicals

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

Deadline for manuscript submissions: 20 May 2025 | Viewed by 7180

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Prof. Dr. Efthymia Kitraki

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Guest Editor

Department of Basic Sciences, Faculty of Dentistry, National and Kapodistrian University of Athens, Athens, Greece
Interests: neuroendocrinology of stress; endocrine disruptors; dental pulp cells

Special Issue Information

Dear Colleagues,

Endocrine-Disrupting Chemicals (EDCs) are artificial compounds that intervene in normal hormone functions through agonistic, antagonistic or disruptive effects. Their actions extend from humans to many other species and are characterized by non-monotonic effects in multiple systems of the exposed organism, as well as transgenerational transfer. Experimental and epidemiological studies indicate that early life exposures are considered more harmful and life-long due to immature defence mechanisms of the organisms, though exposures in adulthood can also have adverse outcomes. Research on the impact of single EDCs has contributed to our understanding of the targets and mechanisms of action of these chemicals. However, it has been shown that co-exposure to more than one EDC can have different effects, compared to single exposures. Nowadays, it is thus well accepted that investigation of the impact of epidemiology-based mixtures of EDCs, instead of single chemicals, is closer to real life conditions. Knowledge on EDCs is rapidly expanding to all aforementioned directions. This Issue aims to provide recent evidence from both cohort studies and experimental models on EDCs or their mixtures, regarding their biomonitoring, target tissues, mechanisms of action, and risk assessment approaches.

Prof. Dr. Efthymia Kitraki
Guest Editor

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Keywords

Endocrine-Disrupting Chemicals (EDCs)
chemical mixtures
biomonitoring
cohort studies
in vivo and in vitro models
mechanisms of action
risk assessment

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Published Papers (5 papers)

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Research

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21 pages, 2910 KiB

Open AccessArticle

Bisphenol a Disrupts Steroidogenesis and Induces Apoptosis in Human Granulosa Cells Cultured In Vitro

by Dominika Celar Šturm, Tadeja Režen, Nina Jančar and Irma Virant-Klun

Int. J. Mol. Sci. 2025, 26(9), 4081; https://doi.org/10.3390/ijms26094081 - 25 Apr 2025

Abstract

Bisphenol A (BPA) is a common synthetic chemical compound classified as an endocrine disruptor. It affects multiple physiological systems in the body, including the female reproductive system, particularly granulosa cells (GCs) in the ovaries, where steroidogenesis occurs. This study investigated the impact of various BPA concentrations (environmentally relevant concentrations of 0.001 µM and 0.1 µM and toxicological concentration of 100 µM) and exposure times (24 and 72 h) on cell viability and counts and in vitro production of estradiol and progesterone in human GCs collected from waste follicular fluid of IVF patients. Gene expression analysis of 182 genes associated with steroidogenesis and apoptosis was performed in GCs using PCR arrays, followed by protein expression analysis by Western blot. Our results demonstrate that after longer BPA exposure (72 h), a higher concentration of BPA (100 µM) negatively affects the cellular viability and counts and significantly alters steroid hormone biosynthesis in vitro, leading to reduced concentrations of estradiol and progesterone in the culture medium. We found that all BPA concentrations altered the expression of different steroidogenesis- and apoptosis-related genes in GCs. At 0.001 μM, BPA exposure decreased the expression of TRIM25, UGT2B15, CASP3, and RPS6KA3 genes and increased the expression of NR6A1 and PPID genes. At 0.1 μM, BPA increased the expression of AR, HSD3B1, BID, IKBKG, and PPID genes while reducing the expression of TRIM25 and CASP3 genes. At the highest concentration of 100 μM, BPA upregulated the expression of AR, GPER30, BID, IKBKG, and PPID genes and downregulated the expression of FOXO1 and UGT2B15 genes. These results highlight BPA’s concentration-specific effects on steroidogenesis and apoptosis and show its potential to compromise GC function, with possible negative implications for female fertility and ovarian health, even at environmentally relevant concentrations. Full article

(This article belongs to the Special Issue Progress in Research on Endocrine-Disrupting Chemicals)

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16 pages, 2953 KiB

Open AccessArticle

Integrated Analysis of Neuroendocrine and Neurotransmission Pathways Following Developmental Atrazine Exposure in Zebrafish

by Sydney C. Stradtman, Jenna N. Swihart, Kaylin Moore, Isabelle N. Akoro, Janiel K. Ahkin Chin Tai, Wagner Antonio Tamagno and Jennifer L. Freeman

Int. J. Mol. Sci. 2024, 25(23), 13066; https://doi.org/10.3390/ijms252313066 - 5 Dec 2024

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Abstract

Atrazine is an endocrine-disrupting herbicide, with exposure impacting adverse outcomes along multiple endocrine pathways. This study investigated the neuroendocrine system as the central target of atrazine toxicity, examining effects of early developmental exposures on neurohormones and genes associated with kisspeptin, hypothalamic, pituitary, and dopamine systems. Zebrafish were exposed to 0, 0.3, 3, or 30 ppb (µg/L) atrazine during two developmental time windows. For neurohormone assessments, exposure was ceased at the end of embryogenesis (72 h post-fertilization, hpf) and analyzed immediately or grown to 0.5, 2, or 2.5 years post-fertilization (ypf). Gene expression was measured immediately after 1–72 hpf or 72–120 hpf exposure. Estradiol decreased in the 0.3 and 30 ppb groups in 0.5 ypf female brains, while dopamine decreased in the same treatment groups at 72 hpf. Increases were also observed in 2.5 ypf female brains (3 ppb) for estradiol and in 2 ypf female and male brains (3 and 30 ppb) for dopamine. Gene expression alterations occurred for the follicle-stimulating hormone (fsh) at 72 hpf and the growth hormone (gh1) at 72 and 120 hpf. Overall, results indicated that developmental atrazine exposure has immediate and long-term sex-specific effects on neurohormonal systems. Full article

(This article belongs to the Special Issue Progress in Research on Endocrine-Disrupting Chemicals)

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14 pages, 10763 KiB

Open AccessArticle

Prenatal Exposure to a Human Relevant Mixture of Endocrine-Disrupting Chemicals Affects Mandibular Development in Mice

by Vagelis Rinotas, Antonios Stamatakis, Athanasios Stergiopoulos, Carl-Gustaf Bornehag, Joëlle Rüegg, Marietta Armaka and Efthymia Kitraki

Int. J. Mol. Sci. 2024, 25(22), 12312; https://doi.org/10.3390/ijms252212312 - 16 Nov 2024

Cited by 1 | Viewed by 2162

Abstract

Mandible is a bony structure of neuroectodermal origin with unique characteristics that support dentition and jaw movements. In the present study, we investigated the effects of gestational exposure to a mixture of endocrine-disrupting chemicals (EDCs) on mandibular growth in mice. The mixture under study (Mixture N1) has been associated with neurodevelopmental effects in both a human cohort and animal studies. Pregnant mice were exposed throughout gestation to 0.5× (times of pregnant women’s exposure levels), 10×, 100× and 500× of Mixture N1, or the vehicle, and the mandibles of the male offspring were studied in adulthood. Micro-CT analysis showed non-monotonic effects of Mixture N1 in the distances between specific mandibular landmarks and in the crown width of M1 molar, as well as changes in the mandibular bone characteristics. The alveolar bone volume was reduced, and the trabecular separation was increased in the 500× exposed mice. Bone volume in the condyle head was increased in all treated groups. Τhe Safranin-O-stained area of mature hypertrophic chondrocytes and the width of their zones were reduced in 0.5×, 10× and 100× exposed groups. This is the first indication that prenatal exposure to an epidemiologically defined EDC mixture, associated with neurodevelopmental impacts, can also affect mandibular growth in mammals. Full article

(This article belongs to the Special Issue Progress in Research on Endocrine-Disrupting Chemicals)

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16 pages, 1460 KiB

Open AccessArticle

SOCS3 Methylation Partially Mediated the Association of Exposure to Triclosan but Not Triclocarban with Type 2 Diabetes Mellitus: A Case-Control Study

by Qian Gao, Changsheng Huan, Zexin Jia, Qingqing Cao, Pengcheng Yuan, Xin Li, Chongjian Wang, Zhenxing Mao and Wenqian Huo

Int. J. Mol. Sci. 2024, 25(22), 12113; https://doi.org/10.3390/ijms252212113 - 11 Nov 2024

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Abstract

This study aimed to evaluate the association of TCs (triclosan (TCS) and triclocarban) exposure with T2DM and glucose metabolism-related indicators and the mediating effect of SOCS3 methylation on their associations. A total of 956 participants (330 T2DM and 626 controls) were included in this case-control study. Logistic regression and generalized linear models were used to assess the effect of TCs on T2DM and glucose metabolism-related indicators. The dose–response relationship between TCs and T2DM was analyzed by restricted cubic spline. Finally, after evaluating the association between TCs and SOCS3 methylation levels, the mediating effect of SOCS3 methylation on the TC−associated T2DM was estimated. Each 1-unit increase in TCS levels was associated with a 13.2% increase in the risk of T2DM (OR = 1.132, 95% CI: 1.062, 1.207). A linear dose–response relationship was found between TCS and T2DM. TCS was negatively associated with Chr17:76356190 methylation. Moreover, mediation analysis revealed that Chr17:76356190 methylation mediated 14.54% of the relationship between TCS exposure and T2DM. Exposure to TCS was associated with a higher prevalence of T2DM. SOCS3 methylation partially mediated the association of TCS with T2DM. Our findings may provide new insights into the treatment of T2DM, and the study of the biological mechanisms of T2DM. Full article

(This article belongs to the Special Issue Progress in Research on Endocrine-Disrupting Chemicals)

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Review

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24 pages, 1073 KiB

Open AccessReview

The Influence of Environmental Exposure to Xenoestrogens on the Risk of Cancer Development

by Martyna Gachowska, Alicja Dąbrowska, Bartosz Wilczyński, Jacek Kuźnicki, Natalia Sauer, Wojciech Szlasa, Christopher Kobierzycki, Zofia Łapińska and Julita Kulbacka

Int. J. Mol. Sci. 2024, 25(22), 12363; https://doi.org/10.3390/ijms252212363 - 18 Nov 2024

Cited by 2 | Viewed by 1905

Abstract

Xenoestrogens (XEs) are a group of exogenous substances that may interfere with the functioning of the endocrine system. They may mimic the function of estrogens, and their sources are plants, water or dust, plastic, chemical agents, and some drugs. Thus, people are highly exposed to their actions. Together with the development of industry, the number of XEs in our environment increases. They interact directly with estrogen receptors, disrupting the transmission of cellular signals. It is proven that XEs exhibit clinical application in e.g., menopause hormone therapy, but some studies observed that intense exposure to XEs leads to the progression of various cancers. Moreover, these substances exhibit the ability to cross the placental barrier, therefore, prenatal exposure may disturb fetus development. Due to the wide range of effects resulting from the biological activity of these substances, there is a need for this knowledge to be systematized. This review aims to comprehensively assess the environmental sources of XEs and their role in increasing cancer risk, focusing on current evidence of their biological and pathological impacts. Full article

(This article belongs to the Special Issue Progress in Research on Endocrine-Disrupting Chemicals)

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