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Environmental Arsenic Exposure, Toxicity Mechanism and Its Contribution to Human...
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Environmental Arsenic Exposure, Toxicity Mechanism and Its Contribution to Human Diseases

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

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 6766

Special Issue Editors

Prof. Dr. Aihua Zhang

E-Mail Website
Guest Editor
The Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, School of Public Health, Guizhou Medical University, Guiyang, China
Interests: arsenic; toxicity mechanism; epigenetic; metabolic disorder; risk assessment; edible and medicinal resource; prevention and treatment
Dr. Xiong Chen

E-Mail Website
Guest Editor
The Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, School of Public Health, Guizhou Medical University, Guiyang, China
Interests: heavy metals; toxicity mechanism; liver damage; early-warning biomarkers; ginkgo biloba
Dr. Dapeng Wang

E-Mail Website
Guest Editor
The Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, School of Public Health, Guizhou Medical University, Guiyang, China
Interests: arsenic toxicity; liver damage; thyroid dysfunction; Vitamin D; inflammatory response; pyroptosis
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; biomarker

Special Issue Information

Dear Colleagues,

Arsenic is a naturally occurring metalloid with wide distribution in the atmosphere, water, coal, soil and even agricultural products and drugs. Tens of millions people around the globe are exposed to potentially toxic levels of arsenic annually, and arsenic exposure has become an established public health issue. Long-term consumption of arsenic-contaminated water or intake of arsenic-contaminated food may cause multiple organs or tissues damage and a variety of diseases, such as skin lesions, cardiovascular disease, diabetes, chronic liver disease and neurodegenerative disorders. In recent years, studies into the toxicity mechanism of arsenic have made considerable progress, including against oxidative stress, inflammatory response, mitochondrial dysfunction, epigenetic regulation, etc. However, so far, the toxicity mechanism of arsenic and its contribution to human diseases remain largely unknown.

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

  1. Metabolism and toxicity of arsenic;
  2. Adverse effects and toxicity mechanism of arsenic on organs;
  3. Early-warning biomarkers for adverse effects of arsenic on health;
  4. Health risk assessment of environmental arsenic exposure;
  5. Prevention and treatment of arsenic-induced toxic effect by edible and medicinal resource.

We cordially invite you to submit your original research papers and reviews.

Prof. Dr. Aihua Zhang
Dr. Xiong Chen
Dr. Dapeng Wang
Prof. Dr. Yanmei Yang
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
  • toxicity mechanism
  • human health
  • arsenic metabolism
  • target organ toxicity
  • risk assessment
  • edible and medicinal resource
  • prevention and treatment

Published Papers (6 papers)

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Research

13 pages, 282 KiB  
Article
Positive Association of Urinary Dimethylarsinic Acid (DMAV) with Serum 25(OH)D in Adults Living in an Area of Water-Borne Arsenicosis in Shanxi, China
by Kunyu Zhang, Yunyi Yin, Man Lv, Xin Zhang, Meichen Zhang, Jia Cui, Ziqiao Guan, Xiaona Liu, Yang Liu, Yanhui Gao and Yanmei Yang
Toxics 2024, 12(1), 83; https://doi.org/10.3390/toxics12010083 - 18 Jan 2024
Viewed by 883
Abstract
Limited studies have demonstrated that inorganic arsenic exposure is positively associated with serum vitamin D levels, although the correlation between urinary arsenic species and serum vitamin D has not been investigated in areas of water-borne arsenicosis. A cross-sectional study of 762 participants was [...] Read more.
Limited studies have demonstrated that inorganic arsenic exposure is positively associated with serum vitamin D levels, although the correlation between urinary arsenic species and serum vitamin D has not been investigated in areas of water-borne arsenicosis. A cross-sectional study of 762 participants was conducted in Wenshui Country, Shanxi Province, a water-borne arsenicosis area. The results showed a positive relationship between urinary arsenic species (inorganic arsenic (iAs), methylarsonic acid (MMAV), dimethylarsinic acid (DMAV) and serum 25(OH)D. Log-binomial regression analysis indicated a 0.4% increase in the risk of vitamin D excess for every 1-unit increment in the Box–Cox transformed urinary DMAV after adjustment for covariates. After stratifying populations by inorganic arsenic methylation metabolic capacity, serum 25(OH)D levels in the populations with iAs% above the median and primary methylation index (PMI) below the median increased by 0.064 ng/mL (95% CI: 0.032 to 0.096) for every one-unit increase in the Box–Cox transformed total arsenic (tAs) levels. Serum 25(OH)D levels increased by 0.592 ng/mL (95% CI: 0.041 to 1.143) for every one-unit rise in the Box–Cox transformed iAs levels in people with skin hyperkeratosis. Overall, our findings support a positive relationship between urinary arsenic species and serum 25(OH)D. It was recommended that those residing in regions with water-borne arsenicosis should take moderate vitamin D supplements to avoid vitamin D poisoning. Full article
(This article belongs to the Special Issue Environmental Arsenic Exposure, Toxicity Mechanism and Its Contribution to Human Diseases)
16 pages, 6406 KiB  
Article
Subchronic Arsenic Exposure Induces Behavioral Impairments and Hippocampal Damage in Rats
by Fang Chu, Wenjing Yang, Yang Li, Chunqing Lu, Zhe Jiao, Keming Bu, Zhipeng Liu, Hongna Sun and Dianjun Sun
Toxics 2023, 11(12), 970; https://doi.org/10.3390/toxics11120970 - 30 Nov 2023
Cited by 1 | Viewed by 1094
Abstract
This study investigated the effects of subchronic arsenic exposure on behavior, neurological function, and hippocampal damage in rats. Thirty-two male Wistar rats were divided into four groups and exposed to different concentrations of arsenic in their drinking water for 12 weeks, while weekly [...] Read more.
This study investigated the effects of subchronic arsenic exposure on behavior, neurological function, and hippocampal damage in rats. Thirty-two male Wistar rats were divided into four groups and exposed to different concentrations of arsenic in their drinking water for 12 weeks, while weekly water intake and body weight were recorded. Various neurobehavioral tests were conducted, evaluating overall activity levels, exploratory behavior, short-term memory, spatial learning and memory, anxiety-like behavior, and depressive-like states. Arsenic levels in urine, serum, and brain tissue were measured, and histopathological analysis assessed hippocampal damage using hematoxylin and eosin staining. The results demonstrated that arsenic exposure did not significantly affect overall activity or exploratory behavior. However, it impaired short-term memory and spatial learning and memory functions. Arsenic-exposed rats exhibited increased anxiety-like behavior and a depressive-like state. Arsenic levels increased dose-dependently in urine, serum, and brain tissue. The histopathological examinations revealed significant hippocampal damage, including neuronal shrinkage, cell proliferation, irregular structure, disordered arrangement, and vacuolation. These findings emphasize the importance of understanding the impact of arsenic exposure on behavior and brain health, highlighting its potential neurological consequences. Full article
(This article belongs to the Special Issue Environmental Arsenic Exposure, Toxicity Mechanism and Its Contribution to Human Diseases)
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16 pages, 9448 KiB  
Article
Unveiling the LncRNA-miRNA-mRNA Regulatory Network in Arsenic-Induced Nerve Injury in Rats through High-Throughput Sequencing
by Fang Chu, Chunqing Lu, Zhe Jiao, Wenjing Yang, Xiyue Yang, Hao Ma, Hao Yu, Sheng Wang, Yang Li, Dianjun Sun and Hongna Sun
Toxics 2023, 11(12), 953; https://doi.org/10.3390/toxics11120953 - 22 Nov 2023
Viewed by 1028
Abstract
Arsenic is a natural toxin which is widely distributed in the environment, incurring diverse toxicities and health problems. Previous studies have shown that long non-coding RNAs (LncRNAs) are also reported to contribute to As-induced adverse effects. LncRNAs are involved in the development of [...] Read more.
Arsenic is a natural toxin which is widely distributed in the environment, incurring diverse toxicities and health problems. Previous studies have shown that long non-coding RNAs (LncRNAs) are also reported to contribute to As-induced adverse effects. LncRNAs are involved in the development of nerve injury, generally acting as sponges for microRNAs (miRNAs). This study aimed to investigate the competitive endogenous RNA (ceRNA) regulatory networks associated with arsenic-induced nerve damage. A total of 40 male Wistar rats were exposed to different doses of arsenic for 12 weeks, and samples were collected for pathological observation and high-throughput sequencing. The ceRNA network was constructed using Cytoscape, and key genes were identified through the PPI network and CytoHubba methods. A real-time quantitative PCR assay was performed to validate gene expression levels. The results showed that subchronic exposure to arsenic in drinking water resulted in pathological and ultrastructural damage to the hippocampal tissue, including changes in neuron morphology, mitochondria, and synapses. Exposure to arsenic results in the dysregulation of LncRNA and mRNA expression in the hippocampal tissues of rats. These molecules participated in multiple ceRNA axes and formed a network of ceRNAs associated with nerve injury. This study also verified key molecules within the ceRNA network and provided preliminary evidence implicating the ENRNOT-00000022622-miR-206-3p-Bdnf axis in the mechanism of neural damage induced by arsenic in rats. These findings provide novel insights into the underlying mechanism of nervous system damage induced by arsenic exposure. Full article
(This article belongs to the Special Issue Environmental Arsenic Exposure, Toxicity Mechanism and Its Contribution to Human Diseases)
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16 pages, 6421 KiB  
Article
Subchronic Arsenite Exposure Induced Atrophy and Erythropoietin Sensitivity Reduction in Skeletal Muscle Were Relevant to Declined Serum Melatonin Levels in Middle-Aged Rats
by Xiong Chen, Wanying Chen, Dapeng Wang, Lu Ma, Junyan Tao and Aihua Zhang
Toxics 2023, 11(8), 689; https://doi.org/10.3390/toxics11080689 - 10 Aug 2023
Cited by 2 | Viewed by 934
Abstract
Arsenic is a kind of widespread environmental toxicant with multiorgan-toxic effects, and arsenic exposure is associated with the occurrence and development of many chronic diseases. The influence of environmental arsenic exposure on skeletal muscle, which is a vital organ of energy and glucose [...] Read more.
Arsenic is a kind of widespread environmental toxicant with multiorgan-toxic effects, and arsenic exposure is associated with the occurrence and development of many chronic diseases. The influence of environmental arsenic exposure on skeletal muscle, which is a vital organ of energy and glucose metabolism, has received increasing attention. This study aimed to investigate the types of inorganic arsenic-induced skeletal muscle injury, and the potential regulatory effects of melatonin (MT) and erythropoietin (EPO) in young (3-month-old) and middle-aged (12-month-old) rats. Our results showed that 1 mg/L sodium arsenite exposure for 3 months could accelerate gastrocnemius muscle atrophy and promote the switch of type II fibers to type I fibers in middle-aged rats; however, it did not cause significant pathological changes of gastrocnemius muscle in young rats. In addition, arsenite could inhibit serum MT levels, and promote serum EPO levels but inhibit EPO receptor (EPOR) expression in gastrocnemius muscle in middle-aged rats, while serum MT levels and EPOR expression in gastrocnemius muscle showed an opposite effect in young rats. Importantly, exogenous MT antagonized the arsenite-induced skeletal muscle toxic effect and restored serum EPO and gastrocnemius muscle EPOR expression levels in middle-aged rats. There was a positive correlation among gastrocnemius muscle index, serum MT level, and gastrocnemius muscle EPOR protein level in arsenite-exposed rats. This study demonstrated that inorganic arsenic could accelerate skeletal muscle mass loss and type II fiber reduction in middle-aged rats, which may be related to decreased MT secretion and declined EPO sensitivity in skeletal muscle. Full article
(This article belongs to the Special Issue Environmental Arsenic Exposure, Toxicity Mechanism and Its Contribution to Human Diseases)
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13 pages, 2556 KiB  
Article
PTEN Overexpression Alters Autophagy Levels and Slows Sodium Arsenite-Induced Hepatic Stellate Cell Fibrosis
by Fei Huang, Guanxin Ding, Yanjie Yuan, Lijun Zhao, Wenmeng Ding and Shunhua Wu
Toxics 2023, 11(7), 578; https://doi.org/10.3390/toxics11070578 - 03 Jul 2023
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Abstract
Exposure to inorganic arsenic remains a global public health problem. The liver is the main target organ, leading to arsenic-induced liver fibrosis. Phosphatase and tensin homology deleted on chromosome ten (PTEN) may participate in arsenic-induced liver fibrosis by regulating autophagy, but the exact [...] Read more.
Exposure to inorganic arsenic remains a global public health problem. The liver is the main target organ, leading to arsenic-induced liver fibrosis. Phosphatase and tensin homology deleted on chromosome ten (PTEN) may participate in arsenic-induced liver fibrosis by regulating autophagy, but the exact mechanisms remain unclear. We established a mouse model of arsenic poisoning through their drinking water and a fibrosis model using the human hepatic stellate cell line LX-2 through NaAsO2 exposure for 24 h. Masson staining measured liver fibrosis. The cells were transfected with a PTEN overexpression plasmid. Western blot and qRT-PCR determined the levels of protein/mRNA expression. Fibrosis was evident in both the mouse model and arsenic-exposed LX-2 cells. NaAsO2 upregulated expression of autophagic markers microtubule-associated protein light chain A/B (LC3), recombinant human autophagy effector protein (Beclin-1), and hairy and enhancer of split homolog-1 (HES1), but downregulated PTEN. Alongside this, α-smooth muscle actin (α-SMA) expression was significantly upregulated by NaAsO2. PTEN overexpression altered NaAsO2-induced autophagy and downregulated LC3 and Beclin-1. While Notch1, HES1, α-SMA, and collagen I expression were all downregulated in the NaAsO2 groups. Therefore, PTEN overexpression might decrease autophagy and inhibit fibrosis progression caused by arsenic, and the NOTCH1/HES1 pathway is likely involved. Full article
(This article belongs to the Special Issue Environmental Arsenic Exposure, Toxicity Mechanism and Its Contribution to Human Diseases)
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13 pages, 5146 KiB  
Article
Arsenic-Induced, Mitochondria-Mediated Apoptosis Is Associated with Decreased Peroxisome Proliferator-Activated Receptor γ Coactivator α in Rat Brains
by Bo Ding, Xinbo Ma, Yang Liu, Bangyao Ni, Siqi Lu, Yuting Chen, Xiaona Liu and Wei Zhang
Toxics 2023, 11(7), 576; https://doi.org/10.3390/toxics11070576 - 02 Jul 2023
Cited by 3 | Viewed by 1180
Abstract
Chronic exposure to arsenic in drinking water damages cognitive function, and nerve cell apoptosis is one of the primary characteristics. The damage to mitochondrial structure and/or function is one of the main characteristics of apoptosis. Peroxisome proliferator-activated receptor γ coactivator α (PGC-1α) is [...] Read more.
Chronic exposure to arsenic in drinking water damages cognitive function, and nerve cell apoptosis is one of the primary characteristics. The damage to mitochondrial structure and/or function is one of the main characteristics of apoptosis. Peroxisome proliferator-activated receptor γ coactivator α (PGC-1α) is involved in the regulation of mitochondrial biogenesis, energy metabolism, and apoptosis. In this study, we aimed to study the role of PGC-1α in sodium arsenite (NaAsO2)-induced mitochondrial apoptosis in rat hippocampal cells. We discovered that increased arsenic-induced apoptosis in rat hippocampus increased with NaAsO2 (0, 2, 10, and 50 mg/L, orally via drinking water for 12 weeks) exposure by TUNEL assay, and the structure of mitochondria was incomplete and swollen and had increased lysosomes, lipofuscins, and nuclear membrane shrinkage observed via transmission electron microscopy. Furthermore, NaAsO2 reduced the levels of Bcl-2 and PGC-1α and increased the levels of Bax and cytochrome C expression. Moreover, correlation analysis showed that brain arsenic content was negatively correlated with PGC-1α levels and brain ATP content; PGC-1α levels were negatively correlated with apoptosis rate; and brain ATP content was positively correlated with PGC-1α levels, but no significant correlation between ATP content and apoptosis has been observed in this study. Taken together, the results of this study indicate that NaAsO2-induced mitochondrial pathway apoptosis is related to the reduction of PGC-1α, accompanied by ATP depletion. Full article
(This article belongs to the Special Issue Environmental Arsenic Exposure, Toxicity Mechanism and Its Contribution to Human Diseases)
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