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Molecular Mechanisms of Disease Caused from Environmental Fluoride and Arsenic...
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Molecular Mechanisms of Disease Caused from Environmental Fluoride and Arsenic Exposures

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Human Toxicology and Epidemiology".

Deadline for manuscript submissions: closed (15 April 2025) | Viewed by 4689

Special Issue Editors

Prof. Dr. Yanmei Yang

E-Mail Website
Guest Editor
1. Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin 150081, China
2. Key Lab of Etiology and Epidemiology, Education Bureau of Heilongjiang Province and Ministry of Health (23618504), Harbin 150081, China
Interests: arsenic; carcinogenesis; epigenetic; aerobic glycolysis; fluorosis; SNPs; biomarker
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Xiance Sun

E-Mail Website
Guest Editor
School of Public Health, Dalian Medical University, Dalian 116044, China
Interests: arsenic; toxicity mechanism; diabetes mellitus; oxidative stress
Prof. Dr. Dapeng Wang

E-Mail Website
Guest Editor
Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, School of Public Health, Guizhou Medical University, Guiyang 550025, China
Interests: environmental toxicology; arsenicosis; liver fibrosis; endocrine toxicology; toxic mechanism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Fluoride and arsenic widely exist in the environment. Excess fluoride causes deleterious effects on mineralized tissues (teeth and bones) and soft tissues including cardiovascular system, neurological system, etc. Excess arsenic may cause a variety of diseases, including skin lesions, cardiovascular disease, neurodegenerative disorders, etc. Tens of millions of people around the globe are exposed to potentially toxic levels of fluoride and arsenic, and fluoride and arsenic exposures have become a public health issue.

Recently, research on the toxicity mechanisms of fluoride and arsenic have made some progress. However, the molecular mechanisms underlying the fluoride- and arsenic-induced toxicity and their contribution to human diseases are largely unknown.

This Special Issue will focus on toxic mechanisms, early-warning biomarkers, and targeted treatments for fluoride- and arsenic-induced adverse effects on human health. Research areas may include (but are not limited to) the following:

  1. Adverse effects and mechanisms of fluoride and arsenic on health;
  2. Early-warning biomarkers for adverse effects of fluoride and arsenic on health;
  3. Health risk assessment of environmental fluoride and arsenic exposures;
  4. Targeted treatment for fluoride- and arsenic-induced toxic effects.

We welcome you to submit your original research papers and reviews to this Special Issue.

Prof. Dr. Yanmei Yang
Prof. Dr. Xiance Sun
Prof. Dr. Dapeng Wang
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 100 words) can be sent to the Editorial Office for announcement on this website.

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

  • arsenic
  • fluorine
  • human health
  • toxicity effect
  • toxicity mechanism
  • biomarkers
  • risk assessment

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Published Papers (5 papers)

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12 pages, 248 KiB  
Article
Interactions Between BMP2/BMP4 Gene Polymorphisms and Fluoride Exposure on Essential Hypertension: A Cross-Sectional Study in China
by Yue Gao, Qingbo Wang, Junhua Wu, Yang Liu, Xin Wang, Yanhui Gao and Yanmei Yang
Toxics 2025, 13(2), 126; https://doi.org/10.3390/toxics13020126 - 8 Feb 2025
Viewed by 663
Abstract
(1) Objective: To evaluate the relationship between fluoride exposure, interactions of BMP2/BMP4 gene polymorphisms, and fluoride exposure on essential hypertension. (2) Methods: A cross-sectional study was conducted among 725 participants in a high-fluoride region of Shanxi Province, China. Urinary fluoride concentrations were measured [...] Read more.
(1) Objective: To evaluate the relationship between fluoride exposure, interactions of BMP2/BMP4 gene polymorphisms, and fluoride exposure on essential hypertension. (2) Methods: A cross-sectional study was conducted among 725 participants in a high-fluoride region of Shanxi Province, China. Urinary fluoride concentrations were measured as indicators of fluoride exposure. Hypertension was diagnosed based on standard guidelines. BMP2 (rs1005464) and BMP4 (rs17563) polymorphisms were genotyped. Logistic regression and interaction models were performed to evaluate associations and interactions between fluoride exposure, gene polymorphisms, and hypertension. (3) Results: Higher urinary fluoride concentrations were significantly associated with an increased risk of hypertension, exhibiting a dose-dependent relationship. The rs1005464 (G > A) polymorphism of BMP2 was identified as a protective factor against hypertension in individuals with the AG + AA genotype. Significant interactions were observed between the BMP2 rs1005464 and BMP4 rs17563 polymorphisms, influencing hypertension risk. Additionally, both multiplicative and additive interactions between high fluoride exposure and the BMP4 rs17563 polymorphism were identified, highlighting the combined impact of environmental and genetic factors on hypertension. (4) Conclusions: Fluoride exposure is positively associated with hypertension. BMP2 gene polymorphisms affect the risk of hypertension, and BMP4 gene polymorphisms may modify the impact of fluoride on hypertension. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Disease Caused from Environmental Fluoride and Arsenic Exposures)
14 pages, 3958 KiB  
Article
Sleep Deprivation and Subchronic Arsenite Exposure Synergistically Induced Skeletal Muscle Aging by Disrupting Melatonin and Cortisol Secretion in Mice
by Hongyi Yang, Xingyu Chen, Xuanfeng Yu, Baofei Sun, Junyan Tao and Xiong Chen
Toxics 2025, 13(2), 97; https://doi.org/10.3390/toxics13020097 - 27 Jan 2025
Cited by 1 | Viewed by 836
Abstract
In recent years, the influence of environmental factors on organismal aging has garnered increasing attention. Studies have shown that sleep deprivation and environmental pollutants could accelerate the emergence of multiple organismal aging phenotypes. In addition, studies have shown that chronic exposure to sodium [...] Read more.
In recent years, the influence of environmental factors on organismal aging has garnered increasing attention. Studies have shown that sleep deprivation and environmental pollutants could accelerate the emergence of multiple organismal aging phenotypes. In addition, studies have shown that chronic exposure to sodium arsenite (iAs) induces skeletal muscle atrophy and the inhibition of melatonin secretion in rats. This study aimed to reveal the synergistic effect of sleep deprivation and arsenite exposure on skeletal muscle aging, including reduced limb grip strength and skeletal muscle mass, along with the serum levels of melatonin (MT) and cortisol (COR) in C57BL/6J mice. The results demonstrated that while exposure to arsenite for 12 weeks or sleep deprivation (SD) for 4 weeks did not exert significant effects on limb grip strength or skeletal muscle mass, their combination exhibited a synergistic effect on skeletal muscle aging. Notably, the iAs+SD group exhibited a significant decline in limb grip strength by Week 12, accompanied by a reduced gastrocnemius muscle mass and muscle index. The pathological analysis showed muscle fiber atrophy, a shift towards slow-twitch muscle fibers (type I), and shortened telomere length. Additionally, oxidative damage was increased in the SD and iAs+SD groups, with decreased levels of SOD and GPx and elevated levels of MDA in the iAs+SD group. The serum MT level and MT/COR ratio were significantly reduced, while the serum COR level was elevated in the iAs+SD group compared to the other groups. A correlation analysis further revealed that the serum MT level and the MT/COR ratio were positively correlated with limb grip strength, muscle index, and telomere length, whereas the serum COR level exhibited negative correlations with these parameters. These findings suggest that sleep deprivation and subchronic exposure to arsenite synergistically induce skeletal muscle aging, and that the disruption of the balance between MT and COR potentially serves as a significant risk factor. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Disease Caused from Environmental Fluoride and Arsenic Exposures)
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21 pages, 2977 KiB  
Article
Fluoride-Mediated Immune Damage Through Cytokine Network Regulation of Tregs
by Bingshu Liu, Siqi Zhu, Qiong Zhang, Fengyu Xie, Dan Wei, Guiyu Fu, Liu Yang, Yanhui Gao and Wei Wei
Toxics 2025, 13(2), 95; https://doi.org/10.3390/toxics13020095 - 26 Jan 2025
Cited by 1 | Viewed by 709
Abstract
Long-term fluoride exposure can induce inflammatory responses in various tissues of the body, thereby affecting the inflammatory microenvironment. To explore how fluoride induces changes in immune function within this microenvironment, this study collected baseline information and biological samples from participants in areas with [...] Read more.
Long-term fluoride exposure can induce inflammatory responses in various tissues of the body, thereby affecting the inflammatory microenvironment. To explore how fluoride induces changes in immune function within this microenvironment, this study collected baseline information and biological samples from participants in areas with the drinking water type of fluorosis, and simultaneously established Wistar rat models with a 12-week and 24-week fluoride exposure, as well as a 12-week fluoride exposure followed by 12-week pure water feeding regimen. Luminex multiplex assays and enzyme-linked immunosorbent assays (ELISAs) were used to measure cytokine expression levels. Subsequently, correlation analysis, multiple linear regression, and mediation analysis were employed to explore the long-term effects induced by the complex cytokine network during fluoride exposure. The population survey results indicated that fluoride suppressed the expression of pro-inflammatory factors such as Interleukin-2 (IL-2), Interleukin-12 (IL-12), Interferon-γ (IFN-γ), Tumor necrosis factor-α (TNF-α), and anti-inflammatory factors such as Interleukin-4 (IL-4), Interleukin-13 (IL-13), and Interleukin-37 (IL-37), while promoting an increase in the proportion of regulatory T cells (Tregs) in peripheral blood. Among these, IL-2 and IFN-γ mediated the fluoride-induced peripheral Tregs expansion. Animal experiments indicate that the proportion of Tregs in peripheral blood and immune organs increases in a time-dependent manner with fluoride exposure. After reducing the fluoride concentration in the drinking water of rats, the number of Tregs remained significantly elevated. The changes in Treg numbers in the 12-week fluoride feeding group, 24-week fluoride feeding group, and 12-week fluoride feeding followed by 12-week water improvement group were related to the cytokine levels. Therefore, the impact of fluoride on the immune homeostasis has cumulative and long-term effects, and may be related to the accumulation and migration of Tregs induced by fluoride in an inflammatory environment, mediated by cytokines. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Disease Caused from Environmental Fluoride and Arsenic Exposures)
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21 pages, 8373 KiB  
Article
Analysis of Acute and Short-Term Fluoride Toxicity in Zebrafish Embryo and Sac–Fry Stages Based on Bayesian Model Averaging
by Tingxu Jin, Xiumei Yang, Yuanhui Zhu, Cheng Yan, Rui Yan, Qianlei Yang, Hairu Huang and Yan An
Toxics 2024, 12(12), 902; https://doi.org/10.3390/toxics12120902 - 11 Dec 2024
Viewed by 1055
Abstract
Acute and short-term toxicity tests are foundational to toxicology research. These tests offer preliminary insights into the fundamental toxicity characteristics of the chemicals under evaluation and provide essential data for chronic toxicity assessments. Fluoride is a common chemical in aquatic environments; however, the [...] Read more.
Acute and short-term toxicity tests are foundational to toxicology research. These tests offer preliminary insights into the fundamental toxicity characteristics of the chemicals under evaluation and provide essential data for chronic toxicity assessments. Fluoride is a common chemical in aquatic environments; however, the findings of toxicological data, such as LC50 for aquatic organisms, often exhibit inconsistency. Consequently, this study employed zebrafish as a model organism during their early life stages to assess the acute and short-term toxicity of fluoride exposure. Bayesian model averaging was utilized to calculate the LC50/EC50 values and establish baseline concentrations. The results indicated a dose–response relationship between water fluoride concentration and harmful outcomes. The 20 mg/L group was identified as the lowest observed adverse effect level (LOAEL) for the majority of toxicity indicators and warrants special attention. Based on the BBMD model averages, the LC50 of fluoride for 1 to 5 days post-fertilization (dpf) zebrafish was 147.00, 80.80, 61.25, 56.50, and 37.50 mg/L, while the EC50 of cumulative malformation rate for 5 dpf zebrafish was 59.75 mg/L. As the benchmark response (BMR) increased, both the benchmark concentrations (BMCs) and benchmark dose levels (BMDLs) also increased. The research aims to provide essential data for the development of environmental water guidelines and to mitigate ecological risks associated with fluoride in aquatic ecosystems. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Disease Caused from Environmental Fluoride and Arsenic Exposures)
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14 pages, 12039 KiB  
Article
Active Vitamin D Ameliorates Arsenite-Induced Thyroid Dysfunction in Sprague–Dawley Rats by Inhibiting the Toll-like Receptor 4/NF-KappaB-Mediated Inflammatory Response
by Hui Li, Jie Xiang, Qian Song, Ying Jin, Meitong Zhou, Lili Fan and Dapeng Wang
Toxics 2024, 12(12), 887; https://doi.org/10.3390/toxics12120887 - 6 Dec 2024
Cited by 1 | Viewed by 950
Abstract
Arsenic, a well-known environmental endocrine disruptor, exerts interference on the body’s endocrine system. Our previous investigations have demonstrated that chronic exposure to sodium arsenite (NaAsO2) can induce thyroid damage and dysfunction in Sprague–Dawley (SD) rats. Vitamin D (VD) is an indispensable [...] Read more.
Arsenic, a well-known environmental endocrine disruptor, exerts interference on the body’s endocrine system. Our previous investigations have demonstrated that chronic exposure to sodium arsenite (NaAsO2) can induce thyroid damage and dysfunction in Sprague–Dawley (SD) rats. Vitamin D (VD) is an indispensable fat-soluble vitamin that plays a crucial role in maintaining thyroid health. In recent years, numerous studies have demonstrated the association between VD deficiency and the development of various thyroid disorders. However, the precise intervention roles and mechanisms of VD in arsenic-induced thyroid injury remain elusive. This study aimed to investigate the intervention effect of VD on NaAsO2-induced thyroid dysfunction in SD rats. The results demonstrated that exposure to NaAsO2 activates the TLR4/NF-κB signaling pathway in thyroid tissue of rats, leading to apoptosis of thyroid cells and subsequent inflammatory damage and disruption of serum thyroid hormone secretion. Supplementation with TAK-242 (a TLR4 inhibitor) and VD effectively inhibits the activation of the TLR4/NF-κB signaling pathway in rat thyroid tissue exposed to NaAsO2, thereby reducing the inflammatory damage and dysfunction caused by arsenic exposure. In conclusion, the findings of this study offer innovative insights into the application of VD in the prevention and treatment of thyroid dysfunction caused by arsenic exposure. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Disease Caused from Environmental Fluoride and Arsenic Exposures)
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