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Toxicity Mechanism of Emerging Pollutants
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Toxicity Mechanism of Emerging Pollutants

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: 20 November 2024 | Viewed by 7716

Special Issue Editors

Dr. Monika Naumowicz

E-Mail Website
Guest Editor
Laboratory of Bioelectrochemistry, Department of Physical Chemistry, Faculty of Chemistry, University of Bialystok, 15-245 Bialystok, Poland
Interests: lipid membranes; liposomes; emerging pollutant; toxicology
Special Issues, Collections and Topics in MDPI journals
Dr. Joanna Kotyńska

E-Mail Website
Guest Editor
Laboratory of Bioelectrochemistry, Department of Physical Chemistry, Faculty of Chemistry, University of Bialystok, 15-245 Bialystok, Poland
Interests: lipid membranes; liposomes; new pollutants; toxicology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The group of emerging pollutant compounds includes environmental contaminants such as pharmaceuticals, disinfectants, personal care products, endocrine disruptors, pesticides, microplastics, and many others. Their impact on human health is often associated with cyto- and genotoxicity, and the effects of their action include diseases such as diabetes, obesity, cancer, circulatory system diseases, and fertility disorders. These substances are detected in the environment in very low concentrations, but they still cause harmful effects on aquatic, soil, and human organisms. That is why it is so important to investigate the mechanisms of their action and discover ways to counteract their toxic properties. The aim of this Special Issue is to collect information on the occurrence, identification, and mechanisms of action of compounds from the emerging pollutants group. This collection of articles will include the most up-to-date articles on the mechanisms of action of environmental contaminants and methods of counteracting the toxicity of various xenobiotics, using the most modern methodologies. Therefore, this Special Issue is open to comprehensive review and original articles and covers the following topics:

  • Emerging pollutants occurrence and identification;
  • Emerging pollutants mechanisms of action;
  • Cytotoxicity and genotoxicity;
  • Molecular mechanisms of xenobiotics activity;
  • Pesticides, microplastic, and cancer;
  • Alleviation of contaminants toxicity.

Dr. Monika Naumowicz
Dr. Joanna Kotyńska
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • emerging pollutant
  • toxicology
  • cancer
  • EDC
  • pesticides
  • microplastic
  • human cell lines
  • environment
  • molecular mechanisms

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Published Papers (6 papers)

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Research

18 pages, 4420 KiB  
Article
Exploring the Effect of Arsenic-Containing Hydrocarbon on the Bidirectional Synaptic Plasticity of the Dorsal Hippocampus
by Chunxiao Tian, Yenan Qi, Yu Zheng, Pei Xia, Qiwen Liu, Mengying Luan, Junyao Zheng, Rujuan Song, Meng Wang, Dejiao Qi, Chan Xiong and Lei Dong
Int. J. Mol. Sci. 2024, 25(13), 7223; https://doi.org/10.3390/ijms25137223 - 29 Jun 2024
Viewed by 1010
Abstract
Arsenic-containing hydrocarbons (AsHCs) are common in marine organisms. However, there is little research on their effects on the central nervous system’s advanced activities, such as cognition. Bidirectional synaptic plasticity dynamically regulates cognition through the balance of long-term potentiation (LTP) and long-term depression (LTD). [...] Read more.
Arsenic-containing hydrocarbons (AsHCs) are common in marine organisms. However, there is little research on their effects on the central nervous system’s advanced activities, such as cognition. Bidirectional synaptic plasticity dynamically regulates cognition through the balance of long-term potentiation (LTP) and long-term depression (LTD). However, the effects of AsHCs on bidirectional synaptic plasticity and the underlying molecular mechanisms remain unexplored. This study provides the first evidence that 15 μg As L−1 AsHC 360 enhances bidirectional synaptic plasticity, occurring during the maintenance phase rather than the baseline phase. Further calcium gradient experiments hypothesize that AsHC 360 may enhance bidirectional synaptic plasticity by affecting calcium ion levels. The enhancement of bidirectional synaptic plasticity by 15 μg As L−1 AsHC 360 holds significant implications in improving cognitive function, treating neuro-psychiatric disorders, promoting neural recovery, and enhancing brain adaptability. Full article
(This article belongs to the Special Issue Toxicity Mechanism of Emerging Pollutants)
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11 pages, 2153 KiB  
Article
Particulate Matter-Induced Neurotoxicity: Unveiling the Role of NOX4-Mediated ROS Production and Mitochondrial Dysfunction in Neuronal Apoptosis
by Ji-Hee Kim, Kyu-Hee Hwang, Seong-Heon Kim, Hi-Ju Kim, Jung-Min Kim, Mi-Young Lee, Seung-Kuy Cha and Jinhee Lee
Int. J. Mol. Sci. 2024, 25(11), 6116; https://doi.org/10.3390/ijms25116116 - 1 Jun 2024
Cited by 1 | Viewed by 855
Abstract
Urban air pollution, a significant environmental hazard, is linked to adverse health outcomes and increased mortality across various diseases. This study investigates the neurotoxic effects of particulate matter (PM), specifically PM2.5 and PM10, by examining their role in inducing oxidative stress and subsequent [...] Read more.
Urban air pollution, a significant environmental hazard, is linked to adverse health outcomes and increased mortality across various diseases. This study investigates the neurotoxic effects of particulate matter (PM), specifically PM2.5 and PM10, by examining their role in inducing oxidative stress and subsequent neuronal cell death. We highlight the novel finding that PM increases mitochondrial ROS production via stimulating NOX4 activity, not through its expression level in Neuro-2A cells. Additionally, PMs provoke ROS production via increasing the expression and activity of NOX2 in SH-SY5Y human neuroblastoma cells, implying differential regulation of NOX proteins. This increase in mitochondrial ROS triggers the opening of the mitochondrial permeability transition pore (mPTP), leading to apoptosis through key mediators, including caspase3, BAX, and Bcl2. Notably, the voltage-dependent anion-selective channel 1 (VDAC1) increases at 1 µg/mL of PM2.5, while PM10 triggers an increase from 10 µg/mL. At the same concentration (100 µg/mL), PM2.5 causes 1.4 times higher ROS production and 2.4 times higher NOX4 activity than PM10. The cytotoxic effects induced by PMs were alleviated by NOX inhibitors GKT137831 and Apocynin. In SH-SY5Y cells, both PM types increase ROS and NOX2 levels, leading to cell death, which Apocynin rescues. Variability in NADPH oxidase sources underscores the complexity of PM-induced neurotoxicity. Our findings highlight NOX4-driven ROS and mitochondrial dysfunction, suggesting a potential therapeutic approach for mitigating PM-induced neurotoxicity. Full article
(This article belongs to the Special Issue Toxicity Mechanism of Emerging Pollutants)
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21 pages, 5194 KiB  
Article
The Influence of Mesotrione on Human Colorectal Adenocarcinoma Cells and Possibility of Its Toxicity Mitigation by Cichoric Acid
by Agata Jabłońska-Trypuć, Urszula Wydro, Elżbieta Wołejko, Monika Kalinowska, Grzegorz Świderski, Rafał Krętowski, Monika Naumowicz, Paweł Kondzior, Marzanna Cechowska-Pasko and Włodzimierz Lewandowski
Int. J. Mol. Sci. 2024, 25(11), 5655; https://doi.org/10.3390/ijms25115655 - 22 May 2024
Cited by 1 | Viewed by 1165
Abstract
Mesotrione, as a widely used herbicide, is present in the environment in detectable amounts, causing serious damage. Here, we aimed to investigate the effect of mesotrione on Caco-2 cells and the possibility of its toxicity mitigation by cichoric acid. Therefore, we analyzed the [...] Read more.
Mesotrione, as a widely used herbicide, is present in the environment in detectable amounts, causing serious damage. Here, we aimed to investigate the effect of mesotrione on Caco-2 cells and the possibility of its toxicity mitigation by cichoric acid. Therefore, we analyzed the cytotoxicity of both these compounds and the selected oxidative stress parameters, apoptosis and interaction of both the tested compounds with the cell membrane and their accumulation within the cells. In cytotoxicity studies, the stimulating activity of mesotrione was observed, and simultaneously, the inhibitory effect of cichoric acid was noticed. This effect was related to the results of oxidative stress analysis and apoptosis measurements. The activity level of key enzymes (glutathione peroxidase, catalase and superoxide dismutase) in Caco-2 cells exposed to cichoric acid was higher as compared to that of the control. The treatment with mesotrione did not induce apoptosis in the Caco-2 cells. The penetration of the studied compounds into the Caco-2 cells was measured by using an HPLC methodology, and the results indicate mesotrione’s high penetration capacity. The distribution of charge on the surface of the cell membranes changed under the influence of both compounds. Considering the mutual interactions of beneficial and potentially toxic food ingredients, it should be noted that, despite the observed favorable trend, cichoric acid is not able to overcome the toxic and cancer-stimulating effects of this pesticide. Full article
(This article belongs to the Special Issue Toxicity Mechanism of Emerging Pollutants)
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24 pages, 4577 KiB  
Article
Manganese and Vanadium Co-Exposure Induces Severe Neurotoxicity in the Olfactory System: Relevance to Metal-Induced Parkinsonism
by Hilary Afeseh Ngwa, Alejandra Bargues-Carot, Huajun Jin, Vellareddy Anantharam, Arthi Kanthasamy and Anumantha G. Kanthasamy
Int. J. Mol. Sci. 2024, 25(10), 5285; https://doi.org/10.3390/ijms25105285 - 13 May 2024
Cited by 1 | Viewed by 1264
Abstract
Chronic environmental exposure to toxic heavy metals, which often occurs as a mixture through occupational and industrial sources, has been implicated in various neurological disorders, including Parkinsonism. Vanadium pentoxide (V2O5) typically presents along with manganese (Mn), especially in welding [...] Read more.
Chronic environmental exposure to toxic heavy metals, which often occurs as a mixture through occupational and industrial sources, has been implicated in various neurological disorders, including Parkinsonism. Vanadium pentoxide (V2O5) typically presents along with manganese (Mn), especially in welding rods and high-capacity batteries, including electric vehicle batteries; however, the neurotoxic effects of vanadium (V) and Mn co-exposure are largely unknown. In this study, we investigated the neurotoxic impact of MnCl2, V2O5, and MnCl2-V2O5 co-exposure in an animal model. C57BL/6 mice were intranasally administered either de-ionized water (vehicle), MnCl2 (252 µg) alone, V2O5 (182 µg) alone, or a mixture of MnCl2 (252 µg) and V2O5 (182 µg) three times a week for up to one month. Following exposure, we performed behavioral, neurochemical, and histological studies. Our results revealed dramatic decreases in olfactory bulb (OB) weight and levels of tyrosine hydroxylase, dopamine, and 3,4-dihydroxyphenylacetic acid in the treatment groups compared to the control group, with the Mn/V co-treatment group producing the most significant changes. Interestingly, increased levels of α-synuclein expression were observed in the substantia nigra (SN) of treated animals. Additionally, treatment groups exhibited locomotor deficits and olfactory dysfunction, with the co-treatment group producing the most severe deficits. The treatment groups exhibited increased levels of the oxidative stress marker 4-hydroxynonenal in the striatum and SN, as well as the upregulation of the pro-apoptotic protein PKCδ and accumulation of glomerular astroglia in the OB. The co-exposure of animals to Mn/V resulted in higher levels of these metals compared to other treatment groups. Taken together, our results suggest that co-exposure to Mn/V can adversely affect the olfactory and nigral systems. These results highlight the possible role of environmental metal mixtures in the etiology of Parkinsonism. Full article
(This article belongs to the Special Issue Toxicity Mechanism of Emerging Pollutants)
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13 pages, 2406 KiB  
Article
Extracellular Vesicles in Environmental Toxicological Studies: Association between Urinary Concentrations of Phthalate Metabolites and Exosomal miRNA Expression Profiles
by Paolo Cocci, Danilo Bondi, Carmen Santangelo, Tiziana Pietrangelo, Vittore Verratti, Angelo Cichelli, Giovanni Caprioli, Franks Kamgang Nzekoue, Manuella Lesly Kouamo Nguefang, Gianni Sagratini, Gilberto Mosconi and Francesco Alessandro Palermo
Int. J. Mol. Sci. 2024, 25(9), 4876; https://doi.org/10.3390/ijms25094876 - 30 Apr 2024
Viewed by 1032
Abstract
Phthalates are chemical compounds, mainly used as additives in plastics, which are known to induce harmful impacts to the environment and human health due to their ability to act as hormone-mimics. Few studies have been reported on the relationship between human exposure to [...] Read more.
Phthalates are chemical compounds, mainly used as additives in plastics, which are known to induce harmful impacts to the environment and human health due to their ability to act as hormone-mimics. Few studies have been reported on the relationship between human exposure to phthalates and the level of circulating microRNAs (miRs), especially those miRs encapsulated in extracellular vesicles/exosomes or exosome-like vesicles (ELVs). We examined the relationship of ELV-miR expression patterns and urine of adult men with five phthalate metabolites (i.e., mono isobutyl phthalate, mono-n-butyl phthalate, mono benzyl phthalate, mono-(2-ethyl-5-oxohexyl) phthalate, mono-(2-ethylhexyl) phthalate) to identify potential biomarkers and relevant pathways. We found significant positive associations which were further confirmed by multivariable analysis. Overall, our analyses showed that the Σ phthalate metabolite concentration was associated with a significant increase in the expression level of two miRs found in ELV: miR-202 and miR-543. Different pathways including cancer and immune-related responses were predicted to be involved in this relationship. Analyzing the specific downstream target genes of miR-202 and miR-543, we identified the phosphatase and tensin homolog (PTEN) as the key gene in several converging pathways. In summary, the obtained results demonstrate that exposure to environmental phthalates could be related to altered expression profiles of specific ELV-miRs in adult men, thereby demonstrating the potential of miRs carried by exosomes to act as early effect biomarkers. Full article
(This article belongs to the Special Issue Toxicity Mechanism of Emerging Pollutants)
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14 pages, 8512 KiB  
Communication
Nanoplastics Penetrate Human Bronchial Smooth Muscle and Small Airway Epithelial Cells and Affect Mitochondrial Metabolism
by Ewa Winiarska, Monika Chaszczewska-Markowska, Daniel Ghete, Marek Jutel and Magdalena Zemelka-Wiacek
Int. J. Mol. Sci. 2024, 25(9), 4724; https://doi.org/10.3390/ijms25094724 - 26 Apr 2024
Viewed by 1495
Abstract
Micro- and nanoplastic particles, including common forms like polyethylene and polystyrene, have been identified as relevant pollutants, potentially causing health problems in living organisms. The mechanisms at the cellular level largely remain to be elucidated. This study aims to visualize nanoplastics in bronchial [...] Read more.
Micro- and nanoplastic particles, including common forms like polyethylene and polystyrene, have been identified as relevant pollutants, potentially causing health problems in living organisms. The mechanisms at the cellular level largely remain to be elucidated. This study aims to visualize nanoplastics in bronchial smooth muscle (BSMC) and small airway epithelial cells (SAEC), and to assess the impact on mitochondrial metabolism. Healthy and asthmatic human BSMC and SAEC in vitro cultures were stimulated with polystyrene nanoplastics (PS-NPs) of 25 or 50 nm size, for 1 or 24 h. Live cell, label-free imaging by holotomography microscopy and mitochondrial respiration and glycolysis assessment were performed. Furthermore, 25 and 50 nm NPs were shown to penetrate SAEC, along with healthy and diseased BSMC, and they impaired bioenergetics and induce mitochondrial dysfunction compared to cells not treated with NPs, including changes in oxygen consumption rate and extracellular acidification rate. NPs pose a serious threat to human health by penetrating airway tissues and cells, and affecting both oxidative and glycolytic metabolism. Full article
(This article belongs to the Special Issue Toxicity Mechanism of Emerging Pollutants)
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