Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
6.4
4.1
Journals
Toxics
Special Issues
Effects and Mechanism of Endocrine Disruption and Reproductive Abnormality of...
share announcement

Effects and Mechanism of Endocrine Disruption and Reproductive Abnormality of Emerging Pollutant

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Reproductive and Developmental Toxicity".

Deadline for manuscript submissions: closed (31 March 2026) | Viewed by 3461

Special Issue Editors

Dr. Liping Lu

E-Mail Website
Guest Editor
School of Public Health, Hangzhou Normal University, Hangzhou 311121, China
Interests: cardiovascular disease; heath risk; endocrine disrupting chemicals; biological mechanism; nuclear receptor pathway
Special Issues, Collections and Topics in MDPI journals
Dr. Yu Han

E-Mail Website
Guest Editor
School of life and Environmental Science, Hangzhou Normal University, Hangzhou, China
Interests: environmental pollution; PFAS; fertilization toxicity; neurotoxicity; immunotoxicology
Dr. Shixuan Cui

E-Mail
Guest Editor
School of Chemistry, Chemical Engineering and Materials Science, Shandong Normal University, Jinan, China
Interests: computational toxicology; theoretical environmental chemistry; toxicity prediction based on machine learning; adverse outcome pathway; interaction between chemicals and nuclear receptors
Dr. Tingjie Zhan

E-Mail Website
Guest Editor
Center for Biological Science and Technology, Advanced Institute of Natural Sciences, Beijing Normal University, Zhuhai, Guangdong 519087, China
Interests: endocrine disrupting chemicals; female reproductive health; in vitro reproductive models; ovarian toxicity; folliculogenesis

Special Issue Information

Dear Colleagues,

Endocrine-disrupting chemicals (EDCs) are widespread exogenous chemicals that can interfere with hormone action and increase the adverse health risks of organisms, including endocrine system disruption, reproductive abnormality, and development impairment. The mechanisms by which biomacromolecule and EDCs exert specific actions have continuously deepened and can provide holistic understandings of adverse endocrine disruption evidence. The Special Issue examines the endocrine-disrupting and reproductive health effects and the potential mechanisms induced by EDC exposure.

The Special Issue focuses on understanding the mechanisms of EDCs’ actions regarding health effects via in vitro, in vivo, and in silico studies, including original articles or reviews. Topics include, but are not limited to, the following examples: (1) investigations of the endocrine disruption or reproductive abnormality of EDCs at various biological levels from molecular mechanisms to health impacts; (2) the determination of the level or dose of EDCs that can induce endocrine disruption; (3) toxicity predictions and mechanism analyses of EDCs utilizing integrated methods of computational toxicology, including molecular simulations and machine learning; (4) the screening and validation of the key biomolecules of EDC-indcued toxic effects based on multi-omics technology; and (5) nuclear receptor-mediated adverse outcomes.

Dr. Liping Lu
Dr. Yu Han
Dr. Shixuan Cui
Dr. Tingjie Zhan
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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. Toxics is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • environmental toxicology
  • endocrine disruption
  • molecular mechanism
  • emerging pollutants
  • nuclear receptor
  • computational toxicology

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

26 pages, 5073 KB  
Article
Differential Effects of Phenanthrene and Its Chlorinated Congeners on Hormone Production and Mitochondrial Function in Ovarian Granulosa Cells
by Genevieve A. Perono, Laiba Jamshed, Rohita Dutt, Reese S. Cameron, James J. Petrik, Philippe J. Thomas and Alison C. Holloway
Toxics 2026, 14(4), 313; https://doi.org/10.3390/toxics14040313 - 7 Apr 2026
Viewed by 1053
Abstract
Halogenated derivatives of polycyclic aromatic hydrocarbons (PAHs), such as chlorinated PAHs (ClPAHs), are an emerging class of contaminants that are being detected in the environment as well as in wildlife and human populations. Previous studies have shown that chemical substitution of PAHs, including [...] Read more.
Halogenated derivatives of polycyclic aromatic hydrocarbons (PAHs), such as chlorinated PAHs (ClPAHs), are an emerging class of contaminants that are being detected in the environment as well as in wildlife and human populations. Previous studies have shown that chemical substitution of PAHs, including chlorination, may alter the toxicity of parent PAHs; however, whether chlorination affects their endocrine-disrupting potential remains unexplored. In this study, we examined the effects of phenanthrene (Phe), one of the most prevalent PAHs, and its chlorinated congeners, 9-chlorophenanthrene (9ClPhe) and 9,10-dichlorophenanthrene (9,10Cl2Phe), on hormone production in granulosa cells, key hormone-secreting cells of the ovary. We observed that Phe and its chlorinated congeners differentially altered anti-Müllerian hormone (AMH), estradiol (E2), and progesterone (P4) secretion. Since mitochondria are central to steroidogenesis, we further evaluated mitochondrial function. While Phe increased ATP production, both 9ClPhe and 9,10Cl2Phe increased ROS, decreased mitochondrial membrane potential, and reduced the expression of markers for mitochondrial dynamics and mitophagy without altering ATP levels. We further tested impacts on cell fate and found that neither Phe nor its chlorinated congeners altered granulosa cell apoptosis. Together, these results suggest that chlorination of Phe leads to dose-dependent, differential effects on hormone production and mitochondrial pathways without inducing cell death in granulosa cells. This study highlights the potential adverse impacts of ClPAH exposure on ovarian follicle development and female fertility by disrupting steroidogenesis and mitochondrial quality control. Full article
(This article belongs to the Special Issue Effects and Mechanism of Endocrine Disruption and Reproductive Abnormality of Emerging Pollutant)
►▼ Show Figures

Graphical abstract

16 pages, 1089 KB  
Article
Association Between Urinary Phthalate Metabolites and Early Spontaneous Abortion
by Lin Tao, Nian Wu, Lulu Dai, Shimin Xiong, Dengqing Liao, Yuanzhong Zhou and Xubo Shen
Toxics 2026, 14(4), 300; https://doi.org/10.3390/toxics14040300 - 30 Mar 2026
Viewed by 712
Abstract
Phthalates (PAEs) are ubiquitous endocrine-disrupting chemicals (EDCs), but their association with early pregnancy loss (gestational age ≤ 12 weeks) remains controversial. This study enrolled pregnant women aged 20–45 years in Zunyi City, China, and included 107 cases and 349 controls following propensity score [...] Read more.
Phthalates (PAEs) are ubiquitous endocrine-disrupting chemicals (EDCs), but their association with early pregnancy loss (gestational age ≤ 12 weeks) remains controversial. This study enrolled pregnant women aged 20–45 years in Zunyi City, China, and included 107 cases and 349 controls following propensity score matching. Logistic regression, restricted cubic spline (RCS) analysis, Bayesian kernel machine regression (BKMR), and weighted quantile sum (WQS) regression were employed to investigate associations between urinary phthalate metabolites and early pregnancy loss. We found that monoethyl phthalate (MEP), mono(2-ethylhexyl) phthalate (MEHP), monooctyl phthalate (MOP), mono(2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) were associated with spontaneous abortion in early pregnancy, with corresponding odds ratios (ORs; 95% confidence intervals [CIs]) of 1.62 (1.26–2.09), 1.49 (1.07–2.09), 1.64 (1.26–2.12), 1.78 (1.27–2.50), 2.63 (1.90–3.64), 1.41 (1.11–1.79), and 5.39 (3.53–8.25). Non-linear dose–response relationships were observed between exposure to MMP, MEP, MEHP, MOP, monobenzyl phthalate (MBZP), MEOHP, MEHHP, and mono-(3-carboxypropyl) phthalate (MECPP) and early pregnancy loss (non-linear p < 0.05; overall p < 0.05). Co-exposure to multiple phthalate metabolites was also linked to a significantly non-linear elevation in the risk of early pregnancy loss (OR; 95% confidence interval [CI]) of 1.92 (1.76–2.15). Among these metabolites, MMP, MOP, MEOHP, and MECPP make the largest contribution to the correlation. In summary, our findings indicate that exposure to phthalate esters during early pregnancy is associated with early pregnancy loss, with MMP, MOP, MEOHP, and MECPP as the primary contributors. However, these results are based on a single urine sample, and caution is warranted when interpreting the findings. Full article
(This article belongs to the Special Issue Effects and Mechanism of Endocrine Disruption and Reproductive Abnormality of Emerging Pollutant)
►▼ Show Figures

Figure 1

13 pages, 1980 KB  
Article
Cardiotoxic Effect Induced by F-53B via Nitric Oxide Signalling on Parkin−/− Mice
by Jun Nie, Chao Hu, Yuru Huang, Ying Ma and Liping Lu
Toxics 2025, 13(11), 942; https://doi.org/10.3390/toxics13110942 - 31 Oct 2025
Viewed by 1206
Abstract
A comprehensive understanding of gene-environment interactions is essential for maintaining human cardiac health, and deficiency in the key parkin gene exacerbates cardiac injury. Per- and polyfluoroalkyl substances (PFAS) exposure has been determined cardiotoxicity from the epidemiological perspective but the potential remained unclear. Here, [...] Read more.
A comprehensive understanding of gene-environment interactions is essential for maintaining human cardiac health, and deficiency in the key parkin gene exacerbates cardiac injury. Per- and polyfluoroalkyl substances (PFAS) exposure has been determined cardiotoxicity from the epidemiological perspective but the potential remained unclear. Here, we investigated the co-effects on cardiac pathological structure and function of an emerging PFAS, 6:2 chlorinated polyfluorinated ether sulfonate acid (F-53B), on male parkin−/− mice at dose of 3 and 3000 μg/kg for 60 d. Mechanism was focused on the activity, phosphorylation of endothelial nitric oxide synthase (eNOS), and the content of nitric oxide (NO), vital vascular function regulating molecule. F-53B significantly increased cardiac fibrosis to 1.58- and 2.80-fold, and cardiac troponin T (cTNT) to 1.17- and 1.32-fold compared with control group, at dose of 3 and 3000 μg/kg, respectively, indicating F-53B can inhibit the normal activities of the heart and cause functional disorders. Content and phosphorylation of eNOS significantly decreased to 0.68-, 0.67-fold, and to 0.65-, 0.54-fold compared with control group, respectively. The subsequent content of NO level was also significantly decreased to 0.47- and 0.33-fold, respectively, indicating that significant co-effects of parkin deficiency and F-53B exposure on cardiac function and structural changes via eNOS/NO signalling. Our work underscores the importance of assessing cardiac risk associated with PFAS at environmentally relevant doses, especially considering environmental exposure and gene co-interaction from the perspective of F-53B and parkin gene. Full article
(This article belongs to the Special Issue Effects and Mechanism of Endocrine Disruption and Reproductive Abnormality of Emerging Pollutant)
►▼ Show Figures

Graphical abstract

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop