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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: closed (20 November 2024) | Viewed by 21113

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Laboratory of Bioelectrochemistry, Department of Physical Chemistry, Faculty of Chemistry, University of Bialystok, 15-245 Bialystok, Poland
Interests: lipid membranes; liposomes; emerging pollutant; toxicology
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Guest Editor
Laboratory of Bioelectrochemistry, Department of Physical Chemistry, Faculty of Chemistry, University of Bialystok, K. Ciolkowskiego 1K, 15-245 Bialystok, Poland
Interests: liposomes; biomimetic membranes; electrokinetic phenomena for membrane charge; microelectrophoresis
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

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Keywords

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

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Related Special Issue

Published Papers (11 papers)

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Research

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16 pages, 4115 KiB  
Article
Polychlorinated Biphenyls Induce Cytotoxicity and Inflammation in an In Vitro Model of an Ocular Barrier
by Alessia Cosentino, Aleksandra Agafonova, Luca Cavallaro, Rosaria Ester Musumeci, Chiara Prinzi, Cinzia Lombardo, Maria Teresa Cambria, Carmelina Daniela Anfuso and Gabriella Lupo
Int. J. Mol. Sci. 2025, 26(3), 916; https://doi.org/10.3390/ijms26030916 - 22 Jan 2025
Cited by 1 | Viewed by 980
Abstract
Polychlorinated biphenyls (PCBs) are heterogeneous, synthetic, and widespread organochlorine compounds, and are one of the persistent organic pollutants present in improperly dumped waste and electronic equipment (e-waste), with a high bioaccumulation potential. In this study, the toxicity of Aroclor 1254 (a mixture of [...] Read more.
Polychlorinated biphenyls (PCBs) are heterogeneous, synthetic, and widespread organochlorine compounds, and are one of the persistent organic pollutants present in improperly dumped waste and electronic equipment (e-waste), with a high bioaccumulation potential. In this study, the toxicity of Aroclor 1254 (a mixture of commercial PCBs) in human corneal epithelial cells (HCEpiCs), in an in vitro model of an ocular barrier, was evaluated. Aroclor 1254 (0.1–10 μg/mL) reduced cell viability, trans-endothelial electric resistance (TEER) and cell migration. Moreover, it induced an inflammatory response, as indicated by the increase in cPLA2 activity, PGE2 production, phosphorylation of ERK 1/2 and p-38, and release of inflammatory cytokines. Aroclor 1254 can damage corneal cells, compromising the integrity of the eye’s outermost barrier. This damage may facilitate the occurrence of infectious processes that are physiologically prevented by the corneal barrier. Full article
(This article belongs to the Special Issue Toxicity Mechanism of Emerging Pollutants)
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20 pages, 14154 KiB  
Article
Differential Cytotoxicity and Inflammatory Responses to Particulate Matter Components in Airway Structural Cells
by Nilofar Faruqui, Sofie Orell, Camilla Dondi, Zaira Leni, Daniel M. Kalbermatter, Lina Gefors, Jenny Rissler, Konstantina Vasilatou, Ian S. Mudway, Monica Kåredal, Michael Shaw and Anna-Karin Larsson-Callerfelt
Int. J. Mol. Sci. 2025, 26(2), 830; https://doi.org/10.3390/ijms26020830 - 20 Jan 2025
Cited by 1 | Viewed by 3486
Abstract
Particulate matter (PM) is a major component of ambient air pollution. PM exposure is linked to numerous adverse health effects, including chronic lung diseases. Air quality guidelines designed to regulate levels of ambient PM are currently based on the mass concentration of different [...] Read more.
Particulate matter (PM) is a major component of ambient air pollution. PM exposure is linked to numerous adverse health effects, including chronic lung diseases. Air quality guidelines designed to regulate levels of ambient PM are currently based on the mass concentration of different particle sizes, independent of their origin and chemical composition. The objective of this study was to assess the relative hazardous effects of carbonaceous particles (soot), ammonium nitrate, ammonium sulfate, and copper oxide (CuO), which are standard components of ambient air, reflecting contributions from primary combustion, secondary inorganic constituents, and non-exhaust emissions (NEE) from vehicular traffic. Human epithelial cells representing bronchial (BEAS-2B) and alveolar locations (H441 and A549) in the airways, human lung fibroblasts (HFL-1), and rat precision-cut lung slices (PCLS) were exposed in submerged cultures to different concentrations of particles for 5–72 h. Following exposure, cell viability, metabolic activity, reactive oxygen species (ROS) formation, and inflammatory responses were analyzed. CuO and, to a lesser extent, soot reduced cell viability in a dose-dependent manner, increased ROS formation, and induced inflammatory responses. Ammonium nitrate and ammonium sulfate did not elicit any significant cytotoxic responses but induced immunomodulatory alterations at very high concentrations. Our findings demonstrate that secondary inorganic components of PM have a lower hazard cytotoxicity compared with combustion-derived and indicative NEE components, and alveolar epithelial cells are more sensitive to PM exposure. This information should help to inform which sources of PM to target and feed into improved, targeted air quality guidelines. Full article
(This article belongs to the Special Issue Toxicity Mechanism of Emerging Pollutants)
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13 pages, 1972 KiB  
Article
PM2.5 Exposure Triggers Hypothalamic Oxidative and ER Stress Leading to Depressive-like Behaviors in Rats
by Hi-Ju Kim, Ji-Hee Kim, Subo Lee, Phuong Anh Do, Ji Yong Lee, Seung-Kuy Cha and Jinhee Lee
Int. J. Mol. Sci. 2024, 25(24), 13527; https://doi.org/10.3390/ijms252413527 - 17 Dec 2024
Cited by 1 | Viewed by 1534
Abstract
Epidemiological studies have linked fine dust pollution to depression, yet the underlying mechanisms remain unclear. Oxidative stress and endoplasmic reticulum (ER) stress are known contributors to depression, but their induction by particulate matter (PM), particularly PM2.5, in animal models has been limited. This [...] Read more.
Epidemiological studies have linked fine dust pollution to depression, yet the underlying mechanisms remain unclear. Oxidative stress and endoplasmic reticulum (ER) stress are known contributors to depression, but their induction by particulate matter (PM), particularly PM2.5, in animal models has been limited. This study aimed to establish a rat model of PM2.5-induced depression-like behaviors and elucidate the underlying molecular mechanisms. Adult male Sprague–Dawley rats received daily intranasal PM2.5 for four weeks. Behavioral assessments, including the open field test (OFT), forced swim test (FST), and light-dark box (LDB) test, were conducted weekly. PM2.5-exposed rats displayed depressive-like behaviors, particularly in the FST, reflecting decreased motivation and learned helplessness. Molecular analyses indicated a specific increase in ER stress markers (CHOP, eIF2α, GRP78, and P16) and NOX4 in the hypothalamus, while other brain regions (striatum, cortex, and hippocampus) were not as pronounced. Additionally, PM2.5 exposure reduced tyrosine hydroxylase (TH) levels in the hypothalamus, suggesting impaired dopamine synthesis. These findings indicate that PM2.5 induces depressive-like behaviors via hypothalamic ER stress and oxidative stress pathways, leading to dopaminergic dysfunction. Targeting oxidative and ER stress within the hypothalamus may offer new therapeutic strategies for treating depression associated with environmental pollutants. Full article
(This article belongs to the Special Issue Toxicity Mechanism of Emerging Pollutants)
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16 pages, 2712 KiB  
Article
In Vitro Investigation of Biological and Toxic Effects of 4-Octylphenol on Human Cells
by Antonio Massimiliano Romanelli, Antonio Montefusco, Silvia Sposito, Bernardina Scafuri, Ivana Caputo and Gaetana Paolella
Int. J. Mol. Sci. 2024, 25(23), 13032; https://doi.org/10.3390/ijms252313032 - 4 Dec 2024
Viewed by 1113
Abstract
Alkylphenols are byproducts of anthropogenic activities that widely contaminate waters, soils and air; among them, the most represented are 4-nonylphenol (4-NP) and 4-octylphenol (4-OP). These compounds tend to bioaccumulate in animal and plant tissues and also represent a risk to human health. Indeed, [...] Read more.
Alkylphenols are byproducts of anthropogenic activities that widely contaminate waters, soils and air; among them, the most represented are 4-nonylphenol (4-NP) and 4-octylphenol (4-OP). These compounds tend to bioaccumulate in animal and plant tissues and also represent a risk to human health. Indeed, humans are constantly exposed to alkylphenols through ingestion of contaminated water and food, inhalation and dermal absorption. In the present work, we characterized the cytotoxic ability of 4-OP towards several human cell lines, representing the potential main targets in the human body, also comparing its effect with that of 4-NP and of a mixture of both 4-OP and 4-NP in a range of concentrations between 1 and 100 μM. Viability assays demonstrated that each cell type had a peculiar sensitivity to 4-OP and that, in some cases, a combination of the two alkylphenols displayed a higher cytotoxic activity with respect to the single compound. Then, we focused our attention on a liver cell line (HepG2) in which we observed that 4-OP increased cell death and also caused interference with protective physiological cell processes, such as the unfolded protein response, autophagy and the antioxidant response. Finally, our experimental data were compared and correlated with ADMET properties originating from an in silico analysis. Altogether, our findings highlight a possible contribution of this pollutant to deregulation of the normal homeostasis in human liver cells. Full article
(This article belongs to the Special Issue Toxicity Mechanism of Emerging Pollutants)
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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 1554
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 6 | Viewed by 1753
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 3 | Viewed by 1790
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 4 | Viewed by 2044
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
Cited by 2 | Viewed by 1557
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
Cited by 8 | Viewed by 2511
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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Review

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43 pages, 12888 KiB  
Review
Marketable and Banned Pesticides in Agriculture: Categorization, Simulation, and Crystallography Review
by Grigorios L. Kyriakopoulos and Ioannis Sebos
Int. J. Mol. Sci. 2024, 25(22), 11885; https://doi.org/10.3390/ijms252211885 - 5 Nov 2024
Cited by 2 | Viewed by 1455
Abstract
Pesticides are playing a dominant role in modern cultivation practices to increase agricultural production but are also criticized for environmental depletion and soil and underground water degradation in field applications. An imperative need for greener pesticides has emerged in alignment with new innovations [...] Read more.
Pesticides are playing a dominant role in modern cultivation practices to increase agricultural production but are also criticized for environmental depletion and soil and underground water degradation in field applications. An imperative need for greener pesticides has emerged in alignment with new innovations in agrarian and agricultural practices. This study provides a comprehensive review of marketable and banned pesticides that have been applied in past times or are still in use in agriculture. The collected literature production disclosed 35 distinct pesticides that were identified either isolated or in mixtures and residues. These pesticides are primarily applied in agricultural fields, but some of them were also criticized for human implications. Then, these 35 pesticides were grouped into four categories: insecticides (18), herbicides (9), fungicides (6), and acaricides (2). Furthermore, their molecular types, chemical structures, pKa or log Kow values were presented. Based on their chemical structure, the pesticides were also organized into two domains: “marketable simulated” and “banned simulated”, representing 43% and 57% of total pesticides, respectively. The simulations were generated by linking the elemental composition of each pesticide in the corresponding category; therefore, three “marketable simulated” (the acaricides were not marketable representative) and four “banned simulated” were demonstrated. In addition, the calculation of “adjustment factors” (−0.33 up to +0.50) and the “as calculated/marketable (or banned) simulated pesticides” ratios (0.946 up to 1.013) enabled the identification of four clusters of homogeneous characteristics: cluster 1: “Insecticides, Fungicides, marketable”, cluster 2: “Herbicides, marketable”, cluster 3: “Insecticides, Fungicides, banned”, and cluster 4: “Acaricides, Herbicides, banned”. Subsequently, the composition of the elements of C and H enabled the crystallography characterization of only the “marketable” pesticides, not those that are “banned”, with compounds that have been already registered in the “Crystallography Open Database”. Conclusively, implications, challenges, and future research recommendations have been proposed. Full article
(This article belongs to the Special Issue Toxicity Mechanism of Emerging Pollutants)
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