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Toxics
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State-of-the-Art Environmental Chemicals Exposomics and Metabolomics
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State-of-the-Art Environmental Chemicals Exposomics and Metabolomics

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Exposome Analysis and Risk Assessment".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 11137

Special Issue Editor

Prof. Dr. Minjian Chen

E-Mail Website
Guest Editor
1. State Key Laboratory of Reproductive Medicine, School of Public Health, Nanjing Medical University, Nanjing 211166, China
2. Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing 211166, China
Interests: metabolomics; exposomics; reproductive and developmental health; exposure science; toxicology

Special Issue Information

Dear Colleagues,

The world's environmental problems are becoming increasingly prominent, and their impacts on human health have attracted widespread attention. Since human exposure is mixed and complex, people are increasingly interested in understanding the relationships between environmental exposures and human health from a broader perspective. This led to the concept of chemical exposome to comprehensively evaluate chemical exposures and their risks. For the high-throughput detection of endogenous chemicals, metabolomics systematically detects endogenous small molecule substrates, intermediates, and products of cell metabolism, which is considered to be closest to the phenotype and provides important information for understanding physiological and pathological processes, and its application in toxicology has great significance. Integrating Environmental Chemicals Exposomics and Metabolomics provides important information for screening out key chemicals leading to impaired outcomes and their toxic metabolic signatures so that the potentially toxic effects of these chemical exposures and underlying mechanisms can be elucidated. This Special Issue focuses on exposomics and metabolomics regarding toxic chemicals and materials, and original research articles, communications, and reviews in this area are welcome.

Dr. Minjian Chen
Guest Editor

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

  • exposomics
  • metabolomics
  • exposome
  • exposure
  • metabolome
  • metabolism
  • health
  • toxicity

Published Papers (7 papers)

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Research

15 pages, 2010 KiB  
Article
Exposure to Molybdate Results in Metabolic Disorder: An Integrated Study of the Urine Elementome and Serum Metabolome in Mice
by Kun Zhou, Miaomiao Tang, Wei Zhang, Yanling Chen, Yusheng Guan, Rui Huang, Jiawei Duan, Zibo Liu, Xiaoming Ji, Yingtong Jiang, Yanhui Hu, Xiaoling Zhang, Jingjing Zhou and Minjian Chen
Toxics 2024, 12(4), 288; https://doi.org/10.3390/toxics12040288 - 14 Apr 2024
Viewed by 547
Abstract
The increasing use of molybdate has raised concerns about its potential toxicity in humans. However, the potential toxicity of molybdate under the current level of human exposure remains largely unknown. Endogenous metabolic alterations that are caused in humans by environmental exposure to pollutants [...] Read more.
The increasing use of molybdate has raised concerns about its potential toxicity in humans. However, the potential toxicity of molybdate under the current level of human exposure remains largely unknown. Endogenous metabolic alterations that are caused in humans by environmental exposure to pollutants are associated with the occurrence and progression of many diseases. This study exposed eight-week-old male C57 mice to sodium molybdate at doses relevant to humans (0.01 and 1 mg/kg/day) for eight weeks. Inductively coupled plasma mass spectrometry (ICP-MS) and ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS) were utilized to assess changes in urine element levels and serum metabolites in mice, respectively. A total of 838 subjects from the NHANES 2017–2018 population database were also included in our study to verify the associations between molybdenum and cadmium found in mice. Analysis of the metabolome in mice revealed that four metabolites in blood serum exhibited significant changes, including 5-aminolevulinic acid, glycolic acid, l-acetylcarnitine, and 2,3-dihydroxypropyl octanoate. Analysis of the elementome revealed a significant increase in urine levels of cadmium after molybdate exposure in mice. Notably, molybdenum also showed a positive correlation with cadmium in humans from the NHANES database. Further analysis identified a positive correlation between cadmium and 2,3-dihydroxypropyl octanoate in mice. In conclusion, these findings suggest that molybdate exposure disrupted amino acid and lipid metabolism, which may be partially mediated by molybdate-altered cadmium levels. The integration of elementome and metabolome data provides sensitive information on molybdate-induced metabolic disorders and associated toxicities at levels relevant to human exposure. Full article
(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)
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17 pages, 1977 KiB  
Article
A Metabolome and Microbiome Analysis of Acute Myeloid Leukemia: Insights into the Carnosine–Histidine Metabolic Pathway
by Binxiong Wu, Yuntian Xu, Miaomiao Tang, Yingtong Jiang, Ting Zhang, Lei Huang, Shuyang Wang, Yanhui Hu, Kun Zhou, Xiaoling Zhang and Minjian Chen
Toxics 2024, 12(1), 14; https://doi.org/10.3390/toxics12010014 - 22 Dec 2023
Viewed by 1269
Abstract
Metabolism underlies the pathogenesis of acute myeloid leukemia (AML) and can be influenced by gut microbiota. However, the specific metabolic changes in different tissues and the role of gut microbiota in AML remain unclear. In this study, we analyzed the metabolome differences in [...] Read more.
Metabolism underlies the pathogenesis of acute myeloid leukemia (AML) and can be influenced by gut microbiota. However, the specific metabolic changes in different tissues and the role of gut microbiota in AML remain unclear. In this study, we analyzed the metabolome differences in blood samples from patients with AML and healthy controls using UPLC-Q-Exactive. Additionally, we examined the serum, liver, and fecal metabolome of AML model mice and control mice using UPLC-Q-Exactive. The gut microbiota of the mice were analyzed using 16S rRNA sequencing. Our UPLC-MS analysis revealed significant differences in metabolites between the AML and control groups in multiple tissue samples. Through cross-species validation in humans and animals, as well as reverse validation of Celastrol, we discovered that the Carnosine–Histidine metabolic pathway may play a potential role in the occurrence and progression of AML. Furthermore, our analysis of gut microbiota showed no significant diversity changes, but we observed a significant negative correlation between the key metabolite Carnosine and Peptococcaceae and Campylobacteraceae. In conclusion, the Carnosine–Histidine metabolic pathway influences the occurrence and progression of AML, while the gut microbiota might play a role in this process. Full article
(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)
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10 pages, 2402 KiB  
Article
The Cytotoxicity of Tungsten Ions Derived from Nanoparticles Correlates with Pulmonary Toxicity
by Jun Yao, Pengfei Zhou, Xin Zhang, Beilei Yuan, Yong Pan and Juncheng Jiang
Toxics 2023, 11(6), 528; https://doi.org/10.3390/toxics11060528 - 13 Jun 2023
Cited by 1 | Viewed by 1283
Abstract
Tungsten carbide nanoparticles (nano-WC) are prevalent in composite materials, and are attributed to their physical and chemical properties. Due to their small size, nano-WC particles can readily infiltrate biological organisms via the respiratory tract, thereby posing potential health hazards. Despite this, the studies [...] Read more.
Tungsten carbide nanoparticles (nano-WC) are prevalent in composite materials, and are attributed to their physical and chemical properties. Due to their small size, nano-WC particles can readily infiltrate biological organisms via the respiratory tract, thereby posing potential health hazards. Despite this, the studies addressing the cytotoxicity of nano-WC remain notably limited. To this purpose, the BEAS-2B and U937 cells were cultured in the presence of nano-WC. The significant cytotoxicity of nano-WC suspension was evaluated using a cellular LDH assay. To investigate the cytotoxic impact of tungsten ions (W6+) on cells, the ion chelator (EDTA-2Na) was used to adsorb W6+ from nano-WC suspension. Subsequent to this treatment, the modified nano-WC suspension was subjected to flow cytometry analysis to evaluate the rates of cellular apoptosis. According to the results, a decrease in W6+ could mitigate the cellular damage and enhance cell viability, which indicated that W6+ indeed exerted a significant cytotoxic influence on the cells. Overall, the present study provides valuable insight into the toxicological mechanisms underlying the exposure of lung cells to nano-WC, thereby reducing the environmental toxicant risk to human health. Full article
(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)
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15 pages, 3952 KiB  
Article
Cigarette Smoke-Induced Gastric Cancer Cell Exosomes Affected the Fate of Surrounding Normal Cells via the Circ0000670/Wnt/β-Catenin Axis
by Zhaofeng Liang, Shikun Fang, Yue Zhang, Xinyi Zhang, Yumeng Xu, Hui Qian and Hao Geng
Toxics 2023, 11(5), 465; https://doi.org/10.3390/toxics11050465 - 17 May 2023
Cited by 1 | Viewed by 1391
Abstract
Cigarette smoke is a major risk factor for gastric cancer. Exosomes are an important part of intercellular and intra-organ communication systems and can carry circRNA and other components to play a regulatory role in the occurrence and development of gastric cancer. However, it [...] Read more.
Cigarette smoke is a major risk factor for gastric cancer. Exosomes are an important part of intercellular and intra-organ communication systems and can carry circRNA and other components to play a regulatory role in the occurrence and development of gastric cancer. However, it is unclear whether cigarette smoke can affect exosomes and exosomal circRNA to promote the development of gastric cancer. Exosomes secreted by cancer cells promote cancer development by affecting surrounding normal cells. Herein, we aimed to clarify whether the exosomes secreted by cigarette smoke-induced gastric cancer cells can promote the development of gastric cancer by affecting the surrounding gastric mucosal epithelial cells (GES-1). In the present study, we treated gastric cancer cells with cigarette smoke extract for 4 days and demonstrated that cigarette smoke promotes the stemness and EMT of gastric cancer cells and cigarette smoke-induced exosomes promote stemness gene expression, EMT processes and the proliferation of GES-1 cells. We further found that circ0000670 was up-regulated in tissues of gastric cancer patients with smoking history, cigarette smoke-induced gastric cancer cells and their exosomes. Functional assays showed that circ0000670 knockdown inhibited the promoting effects of cigarette smoke-induced exosomes on the stemness and EMT characteristic of GES-1 cells, whereas its overexpression had the opposite effect. In addition, exosomal circ0000670 was found to promote the development of gastric cancer by regulating the Wnt/β-catenin pathway. Our findings indicated that exosomal circ0000670 promotes cigarette smoke-induced gastric cancer development, which might provide a new basis for the treatment of cigarette smoke-related gastric cancer. Full article
(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)
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12 pages, 4941 KiB  
Article
Multi-Omics Analyses Reveal the Mechanisms of Early Stage Kidney Toxicity by Diquat
by Huazhong Zhang, Jinsong Zhang, Jinquan Li, Zhengsheng Mao, Jian Qian, Cheng Zong, Hao Sun and Beilei Yuan
Toxics 2023, 11(2), 184; https://doi.org/10.3390/toxics11020184 - 16 Feb 2023
Cited by 2 | Viewed by 1640
Abstract
Diquat (DQ), a widely used bipyridyl herbicide, is associated with significantly higher rates of kidney injuries compared to other pesticides. However, the underlying molecular mechanisms are largely unknown. In this study, we identified the molecular changes in the early stage of DQ-induced kidney [...] Read more.
Diquat (DQ), a widely used bipyridyl herbicide, is associated with significantly higher rates of kidney injuries compared to other pesticides. However, the underlying molecular mechanisms are largely unknown. In this study, we identified the molecular changes in the early stage of DQ-induced kidney damage in a mouse model through transcriptomic, proteomic and metabolomic analyses. We identified 869 genes, 351 proteins and 96 metabolites that were differentially expressed in the DQ-treated mice relative to the control mice (p < 0.05), and showed significant enrichment in the PPAR signaling pathway and fatty acid metabolism. Hmgcs2, Cyp4a10, Cyp4a14 and Lpl were identified as the major proteins/genes associated with DQ-induced kidney damage. In addition, eicosapentaenoic acid, linoleic acid, palmitic acid and (R)-3-hydroxybutyric acid were the major metabolites related to DQ-induced kidney injury. Overall, the multi-omics analysis showed that DQ-induced kidney damage is associated with dysregulation of the PPAR signaling pathway, and an aberrant increase in Hmgcs2 expression and 3-hydroxybutyric acid levels. Our findings provide new insights into the molecular basis of DQ-induced early kidney damage. Full article
(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)
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17 pages, 3724 KiB  
Article
Stage-Related Neurotoxicity of BPA in the Development of Zebrafish Embryos
by Jianjun Liu, Wenyu Kong, Yuchen Liu, Qiyao Ma, Qi Shao, Liwen Zeng, Yu Chao, Xiaoyao Song and Jie Zhang
Toxics 2023, 11(2), 177; https://doi.org/10.3390/toxics11020177 - 14 Feb 2023
Cited by 4 | Viewed by 1650
Abstract
Bisphenol A (BPA) is one of the most widely produced chemicals in the world used in the production of epoxy resins and polycarbonate plastics. BPA is easily migrated from the outer packaging to the contents. Due to the lipophilic property, BPA is easily [...] Read more.
Bisphenol A (BPA) is one of the most widely produced chemicals in the world used in the production of epoxy resins and polycarbonate plastics. BPA is easily migrated from the outer packaging to the contents. Due to the lipophilic property, BPA is easily accumulated in organisms. Perinatal low-dose BPA exposure alters brain neural development in later generations. In this study, after BPA treatment, the spontaneous movement of zebrafish larvae from the cleavage period to the segmentation period (1–24 hpf) was significantly decreased, with speed decreasing by 18.97% and distance decreasing between 18.4 and 29.7% compared to controls. Transcriptomics analysis showed that 131 genes were significantly differentially expressed in the exposed group during the 1–24 hpf period, among which 39 genes were significantly upregulated and 92 genes were significantly downregulated. The GO enrichment analysis, gene function analysis and real-time quantitative PCR of differentially expressed genes showed that the mRNA level of guanine deaminase (cypin) decreased significantly in the 1–24 hpf period. Moreover, during the 1–24 hpf period, BPA exposure reduced guanine deaminase activity. Therefore, we confirmed that cypin is a key sensitive gene for BPA during this period. Finally, the cypin mRNA microinjection verified that the cypin level of zebrafish larvae was restored, leading to the restoration of the locomotor activity. Taken together, the current results show that the sensitive period of BPA to zebrafish embryos is from the cleavage period to the segmentation period (1–24 hpf), and cypin is a potential target for BPA-induced neurodevelopmental toxicity. This study provides a potential sensitive period and a potential target for the deep understanding of neurodevelopmental toxicity mechanisms caused by BPA. Full article
(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)
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11 pages, 1633 KiB  
Article
A UPLC Q-Exactive Orbitrap Mass Spectrometry-Based Metabolomic Study of Serum and Tumor Tissue in Patients with Papillary Thyroid Cancer
by Bo Xu, Wei Gao, Ting Xu, Cuiping Liu, Dan Wu and Wei Tang
Toxics 2023, 11(1), 44; https://doi.org/10.3390/toxics11010044 - 31 Dec 2022
Cited by 2 | Viewed by 1714
Abstract
Objective: To find the metabolomic characteristics of tumor or para-tumor tissues, and the differences in serums from papillary thyroid cancer (PTC) patients with or without lymph node metastasis. Methods: We collected serums of PTC patients with/without lymph node metastasis (SN1/SN0), tumor and adjacent [...] Read more.
Objective: To find the metabolomic characteristics of tumor or para-tumor tissues, and the differences in serums from papillary thyroid cancer (PTC) patients with or without lymph node metastasis. Methods: We collected serums of PTC patients with/without lymph node metastasis (SN1/SN0), tumor and adjacent tumor tissues of PTC patients with lymph node metastasis (TN1 and PN1), and without lymph node metastasis (TN0 and PN0). Metabolite detection was performed by ultra-high performance liquid chromatography combined with Q-Exactive orbitrap mass spectrometry (UPLC Q-Exactive). Results: There were 31, 15, differential metabolites in the comparisons of TN1 and PN1, TN0 and PN0, respectively. Seven uniquely increased metabolites and fourteen uniquely decreased metabolites appeared in the lymph node metastasis (TN1 and PN1) group. Meanwhile, the results indicated that four pathways were co-owned pathways in two comparisons (TN1 and PN1, TN0 and PN0), and four unique pathways presented in the lymph node metastasis (TN1 and PN1) group. Conclusions: Common or differential metabolites and metabolic pathways were detected in the lymph node metastasis and non-metastatic group, which might provide novel ways for the diagnosis and treatment of PTC. Full article
(This article belongs to the Special Issue State-of-the-Art Environmental Chemicals Exposomics and Metabolomics)
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