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Toxics
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State-of-the-Art Environmental Chemical Exposomics and Metabolomics—2nd Edition
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State-of-the-Art Environmental Chemical Exposomics and Metabolomics—2nd Edition

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 2025 | Viewed by 2007

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 Issues, Collections and Topics in MDPI journals

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 has 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 are considered to be closest to the phenotype and provide important information for understanding physiological and pathological processes, and its application in toxicology has great significance. Integrating environmental chemical exposomics and metabolomics provides important information for the screening out of 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. In Volume I, we published papers regarding the development of new methods of chemical-exposome-related detection and applications of metabolomics and its integration with information from exposomics as well as other omics and different biological layers in the toxicological area, advancing our understanding of this topic. This Special Issue focuses on the exposomics of toxic chemicals and materials and metabolomics of endogenous metabolites, and original research articles, communications, and reviews in this area are welcome to be submitted.

Prof. 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

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Published Papers (2 papers)

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Research

14 pages, 3905 KiB  
Article
Acrylamide Induces Antiapoptotic Autophagy and Apoptosis by Activating PERK Pathway in SH-SY5Y Cells
by Yiqi Wang, Ying Liu, Xing Zhang, Yang Jiao, Lian Duan, Ruijie Cheng, Ning Yang and Hong Yan
Toxics 2025, 13(1), 41; https://doi.org/10.3390/toxics13010041 - 7 Jan 2025
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Abstract
Acrylamide (ACR) is a commonly used organic compound that exhibits evident neurotoxicity in humans. Our previous studies showed that the mechanisms of ACR-caused neurotoxicity included apoptosis, PERK-mediated endoplasmic reticulum stress, and autophagy, but the relationships among them were still unclear. This paper investigated [...] Read more.
Acrylamide (ACR) is a commonly used organic compound that exhibits evident neurotoxicity in humans. Our previous studies showed that the mechanisms of ACR-caused neurotoxicity included apoptosis, PERK-mediated endoplasmic reticulum stress, and autophagy, but the relationships among them were still unclear. This paper investigated the relationships among apoptosis, autophagy, and the PERK pathway to demonstrate the mechanism of ACR neurotoxicity further. Different doses of ACR were set to value ACR toxicity. Then, a PERK inhibitor and autophagy inhibitor, GSK2606414 and 3-methyladenine (3-MA), were used separately to inhibit the PERK pathway and autophagy activation in SH-SY5Y cells under ACR treatment. With the increase of ACR dose, the apoptotic rate increased in a dose-dependent manner. After the inhibition of the PERK pathway, the activated apoptosis and autophagosome accumulation caused by ACR were alleviated. Under 3-MA and ACR treatment, the autophagy inhibition deteriorated apoptosis in SH-SY5Y cells but had no significant effect on ACR-induced PERK pathway activation; thus, PERK pathway-induced autophagy had an antiapoptotic role in this condition. This paper provides an experimental basis for exploring potential molecular targets to prevent and control ACR toxicity. Full article
(This article belongs to the Special Issue State-of-the-Art Environmental Chemical Exposomics and Metabolomics—2nd Edition)
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15 pages, 6121 KiB  
Article
Network Toxicology and Molecular Docking Analysis of Tetracycline-Induced Acute Pancreatitis: Unveiling Core Mechanisms and Targets
by Hang Lei, Yimao Wu, Wenjun Ma, Jiaqi Yao, Pengcheng Zhang, Yong Tian, Yuhong Jiang, Zhijun Xie, Lv Zhu and Wenfu Tang
Toxics 2024, 12(12), 929; https://doi.org/10.3390/toxics12120929 - 21 Dec 2024
Viewed by 1043
Abstract
Acute pancreatitis (AP), induced by tetracycline, a widely used antibiotic, poses significant clinical and toxicological challenges, yet its molecular mechanisms remain unclear. This study aims to promote drug toxicology strategies for the effective investigation of the putative toxicity and potential molecular mechanisms of [...] Read more.
Acute pancreatitis (AP), induced by tetracycline, a widely used antibiotic, poses significant clinical and toxicological challenges, yet its molecular mechanisms remain unclear. This study aims to promote drug toxicology strategies for the effective investigation of the putative toxicity and potential molecular mechanisms of antibiotic drugs through the study of tetracycline in AP. Using the SwissTargetPrediction, SEA Search, Super-PRED, GeneCards, Drugbank, Online Mendelian Inheritance in Man (OMIM), and Therapeutic Target Database (TTD), we identified 259 potential targets associated with tetracycline exposure and AP. Further refinement via the STRING database and Cytoscape (version 3.10.1) software highlighted 22 core targets, including TP53, TNF, and AKT1. Functional enrichment via the Database for Annotation, Visualization, and Integrated Discovery (DAVID) identified pathways through Gene Ontology (GO) terms and the Kyoto Encyclopedia of Genes and Genomes (KEGG) database, highlighting PI3K-Akt, MAPK, HIF-1, and AGE-RAGE as critical mediators in tetracycline-induced AP. Molecular docking confirmed the strong binding between tetracycline and the core targets. Overall, these findings suggest that tetracycline may affect the occurrence and progression of pancreas-related inflammation by regulating pancreatic cell apoptosis and proliferation, activating inflammatory signaling pathways, and regulating lipid metabolic pathways. This study provides a theoretical basis for understanding the molecular mechanism of tetracycline-induced AP and lays the foundation for the prevention and treatment of digestive system diseases associated with excessive exposure to tetracycline antibiotics and certain tetracyclines. In addition, our network toxicology approach has accelerated the elucidation of toxic pathways in antibiotic drugs that lack specific characteristics. Full article
(This article belongs to the Special Issue State-of-the-Art Environmental Chemical Exposomics and Metabolomics—2nd Edition)
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