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Molecular Mechanisms of Toxicity Caused by Environmental Pollutants

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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 August 2026 | Viewed by 1808

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Dr. Ivan Girón-Perez

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Guest Editor

Secretaría de Investigación y Posgrado, Laboratorio Nacional CONACyT LANIIA-Nayarit, Universidad Autónoma de Nayarit, Tepic, Mexico
Interests: immunotoxicity; pesticides; cholinergic system; COVID-19 and Immunity; immunomodulation

Special Issue Information

Dear Colleagues,

The Special Issue focuses on the molecular and cellular mechanisms of toxicity caused by classic and emerging environmental pollutants. Studies examining the effects of environmental contaminants on human and animal health (both vertebrate and invertebrate) are welcome. Topics of interest include immunotoxicology, neurotoxicity, and disruption of homeostatic systems by contaminants. Pollutants of primary interest are pesticides, mycotoxins, hydrocarbons, and dioxins, as well as emerging contaminants such as antibiotics, pharmaceuticals, plasticizers (e.g., as bisphenol A), and microplastics. Preference will be given to papers presenting experimental results, although review articles are also welcome.

Dr. Ivan Girón-Perez
Guest Editor

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Keywords

environmental pollutant
molecular toxicity
immunotoxicology
neurotoxicity

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Published Papers (4 papers)

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Research

23 pages, 3663 KB

Open AccessArticle

Mosses and Snails as Bioindicators Reflecting the Biologically Relevant Fraction of Toxic Elements

by Alessia Postiglione, Alessia Di Fraia, Tania Russo, Gianluca Polese, Martina Dentato, Sergio Sorbo, Adriana Basile and Viviana Maresca

Int. J. Mol. Sci. 2026, 27(12), 5225; https://doi.org/10.3390/ijms27125225 (registering DOI) - 9 Jun 2026

Abstract

Air pollution is a major environmental and public health issue, largely driven by human activities. The present study evaluates the combined use of two bioindicators from different taxonomic groups, the moss Rhytidiadelphus squarrosus and the terrestrial snail Cornu aspersum, to assess early biological effects induced by atmospheric exposure to toxic elements. Both species, chosen for their sensitivity, simple physiology, and suitability for field transplantation, were exposed for 30 days at two sites in southern Italy with contrasting environmental conditions. Toxic element accumulation in moss biomass and snail tissues was measured using ICP-OES, while snail shell composition was analyzed using FTIR spectroscopy. Biological responses were assessed through oxidative stress biomarkers (ROS levels and catalase activity), HSP70 expression determined by Western blotting, and structural damage, including ultrastructural changes in mosses and histopathological alterations in snails. Results showed site-dependent patterns of toxic elements accumulation in both organisms, consistent with increased oxidative stress and induction of HSP70 expression. Enlargement of the albumen gland and histological alterations in digestive tubules and reproductive systems were found in snails. Mosses showed severe ultrastructural alterations. FTIR analysis revealed changes in snail shell composition consistent with metal exposure. Principal component analysis highlighted clear patterns linking contamination, oxidative stress, and structural damage, supporting the complementarity of the two bioindicators and their ability to capture distinct exposure pathways and biological effects. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Toxicity Caused by Environmental Pollutants)

21 pages, 7006 KB

Open AccessArticle

PCB 118 Exposure Modulates Chromatin Organization, Ribosome Biogenesis, and Autophagy-Related Pathways in Neuron-like: A Transcriptomic Analysis

by Simone D’Angiolini, Serena Silvestro, Luigi Chiricosta, Michele Scuruchi and Aurelio Minuti

Int. J. Mol. Sci. 2026, 27(11), 5058; https://doi.org/10.3390/ijms27115058 - 3 Jun 2026

Viewed by 195

Abstract

Polychlorinated biphenyls (PCBs) are persistent environmental pollutants associated with neurodevelopmental and neurodegenerative disorders. PCB 118 is one of the most abundant congeners and exerts neurotoxic effects, yet the molecular mechanisms underlying its impact on human neurons remain poorly understood. We investigated the molecular response of retinoic acid-differentiated, neuron-like SH-SY5Y cells exposed to 5 µM PCB 118 for 24 h, a concentration that did not affect cell viability. RNA sequencing identified 1239 differentially expressed genes. Functional enrichment and protein-protein interaction analyses identified upregulation of histone and chromatin structural genes, indicative of substantial chromatin remodeling. In parallel, a significant downregulation of genes involved in ribosome biogenesis and rRNA processing was observed, potentially indicating impairment of the protein synthesis machinery. These transcriptional changes point to a coordinated reprogramming of nuclear architecture and translational machinery, potentially compromising neuronal homeostasis. The modulation of proteostasis-related pathways further supports a mechanistic link between PCB 118 exposure and neuronal dysfunction. Our results provide a comprehensive transcriptional framework connecting PCB 118 to chromatin-mediated gene regulation and suppression of ribosome biogenesis in human neuron-like cells. This study offers mechanistic insights into how environmental PCB exposure may contribute to neurotoxicity and highlights molecular pathways potentially implicated in the development of neurodegenerative disorders. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Toxicity Caused by Environmental Pollutants)

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13 pages, 6420 KB

Open AccessArticle

Forchlorfenuron Exposure Induces Hepatocyte Apoptosis via MKK3/P38/ATF2 Pathway

by Yunqi Zhang, Yun Luo, Xiaoyang Che, Ziru Dai, Xiao Sun and Xiaobo Sun

Int. J. Mol. Sci. 2026, 27(5), 2173; https://doi.org/10.3390/ijms27052173 - 26 Feb 2026

Viewed by 469

Abstract

Forchlorfenuron is a widely used plant cytokinin in Traditional Chinese Medicine and agricultural cultivation to boost resistance, postpone senescence, and increase productivity. However, the improper use of forchlorfenuron results in excessive residues and contamination, raising health and safety concerns. Our research investigated the toxicity of forchlorfenuron on hepatocytes in vitro. Results showed that forchlorfenuron inhibited HepaRG cell viability in a concentration and time-dependent manner. Forchlorfenuron-induced cellular apoptosis and the increased intracellular reactive oxygen species (ROS) indicated the participation of oxidative stress. Molecular docking and network pharmacology data suggested that the hepatotoxicity of forchlorfenuron might involve the MAPK signaling pathway. After 24 h of forchlorfenuron exposure, the P38-MAP kinase, upstream kinases MKK3, and the transcription factor ATF2 were maximally activated. Apoptosis induced by forchlorfenuron was significantly reduced by pretreatment with the P38 inhibitor SB203580. These findings implicated that HepaRG hepatocyte injuries were generated by forchlorfenuron through the induction of cellular apoptosis via the MKK3/P38/ATF2 pathway. Forchlorfenuron application should be closely managed to prevent potential liver damage. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Toxicity Caused by Environmental Pollutants)

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12 pages, 1559 KB

Open AccessArticle

Modulation of Master Transcription Factor Expression of Nile Tilapia Leukocytes via Cholinergic Pathways

by Manuel Ivan Girón-Pérez, Kenia María Ramírez-Ibarra, Carlos Eduardo Covantes-Rosales, Daniel Alberto Girón-Pérez, Francisco Fabián Razura-Carmona, Arturo Contis-Montes de Oca, Jorge Morales-Montor, Lenin Pavón and Gladys Alejandra Toledo-Ibarra

Int. J. Mol. Sci. 2025, 26(22), 11206; https://doi.org/10.3390/ijms262211206 - 20 Nov 2025

Viewed by 618

Abstract

Teleost fish are the first evolutionary group to exhibit an innate and adaptive immune system. Within the mechanisms of adaptive immunity, fish possess, among others, T-helper cells (CD4-like) and their differentiation machinery, regulated by the master transcription factors T-bet, GATA3, Foxp3, and RORγ. Many studies support the existence of a non-neuronal cholinergic system involved in the immune response, named after the ability of leukocytes to synthesize de novo acetylcholine (ACh). Organophosphorus pesticides (OPs), such as diazoxon (DXN), are examples of compounds that act as cholinergic disruptors with immunotoxic effects. The present study aimed to evaluate the expression of transcription factors in leukocytes (spleen mononuclear cells, SMNCs) of Nile tilapia by modulating cholinergic pathways in immune cells using agonists, antagonists, and diazoxon (DXN), an anticholinesterase substance. The obtained data showed a significant increase in RORγ mRNA expression upon stimulation with the nicotinic agonist, whereas activation of the muscarinic receptor with its agonist increased T-bet mRNA expression. An alteration in RORγ expression levels induced by DXN exposure was also observed. The results suggest a probable directing of the immune response towards a pro-inflammatory profile orchestrated mainly by RORγ and T-bet transcription factors in response to cholinergic stimuli. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Toxicity Caused by Environmental Pollutants)

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