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The Influence of Environmental Factors on Disease and Health Outcomes

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 December 2025 | Viewed by 4194

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Guest Editor
Division of Ecology and Environmental Protection, Department of Medical Biology and Biochemistry, Faculty of Medicine, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, M. Skłodowska-Curie St. 9, PL, 85-094 Bydgoszcz, Poland
Interests: environmental effects of condition; ecophysiology; epigenetic impact; environmental biogeochemistry; genetic polymorphisms

Special Issue Information

Dear Colleagues,

According to Tim Spector, Professor of genetic epidemiology, Kings College, London, one of the pioneers of epigenetics, who conducts research into the influence of the environment on DNA, there was a real revolution in genetics: long-standing scientific dogmas said that once we inherit genes, the environment would not change them and we would stay with them until we die. It has recently become known that genes can change as a result of lifestyles, and that these changes can persist and be passed on to future generations. Thanks to recently explored epigenetic processes, genes are turned on and off, so that even twins with identical genotypes can clearly differ from each other.

Environmental external and internal stressors can change epigenetic patterns through DNA methylation, thereby affecting gene activation and cell phenotype. For a long time, DNA methylation analysis was hampered by a lack of a sensitive and high-throughput method. After ions enter the body, a long sequence of chemical reactions begins, causing cell, tissue, or whole-organ dysfunction. Then, external signs of malfunction appear.

Given the increasing threats and impacts of environmental factors (WHO) on human health and disease, it is very important to study the mechanisms and possible preventive measures. Hence this Special Issue aims to comprehensively show the inter-relationships between environmental factors and the reactions of an organism (individual) at the organ, cellular, and subcellular levels. Our goal is to analyze the importance of ecophysiological mechanisms, processes, reactions, and phenomena, as well as their importance in medicine, physiology, and environmental activity in order to prevent the development of environmental abnormalities related to the body’s condition and health. We welcome both full-length and short research original papers, hypothesis papers, reviews, mini reviews etc.

Dr. Piotr Kamiński
Guest Editor

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Keywords

  • environmental factors
  • ecophysiological determinations
  • genetic predispositions
  • gene expression
  • defensive responses
  • pathophysiological abnormalities
  • lifestyle diseases
  • polymorphisms

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Published Papers (3 papers)

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Research

22 pages, 5335 KB  
Article
An Italian Study of PM0.5 Toxicity: In Vitro Investigation of Cytotoxicity, Oxidative Stress, Intercellular Communication, and Extracellular Matrix Metalloproteases
by Nathalie Steimberg, Giovanna Mazzoleni, Jennifer Boniotti, Milena Villarini, Massimo Moretti, Annalaura Carducci, Marco Verani, Tiziana Grassi, Francesca Serio, Sara Bonetta, Elisabetta Carraro, Alberto Bonetti, Silvia Bonizzoni, Umberto Gelatti and the MAPEC_LIFE Study Group
Int. J. Mol. Sci. 2025, 26(14), 6769; https://doi.org/10.3390/ijms26146769 - 15 Jul 2025
Viewed by 312
Abstract
Particulate matter (PM), mainly PM0.5, represents a significant concern for human health, particularly relating to lung homeostasis, and more research is required to ascertain its tissue tropism and the molecular pathways involved. In this study, we first focus on classical in [...] Read more.
Particulate matter (PM), mainly PM0.5, represents a significant concern for human health, particularly relating to lung homeostasis, and more research is required to ascertain its tissue tropism and the molecular pathways involved. In this study, we first focus on classical in vitro toxicological endpoints (cytotoxicity and cell growth) in human bronchial and alveolar epithelial cell lines mimicking the two pulmonary target tissues. Air samples were collected in five Italian cities (Brescia, Lecce, Perugia, Pisa, Turin) during winter and spring. To better decipher the PM0.5 effects on pulmonary cells, a further winter sampling was performed in Brescia, and studies were extended to assess tumour promotion, oxidative stress, and the activity of Matrix metalloproteases (MMP). The results confirmed that the effect of air pollution is linked to the seasons (winter is usually more cytotoxic than spring) and is correlated with the peculiar characteristics of the cities studied (meteoclimatic conditions, economic/anthropogenic activities). Alveolar cells were often less sensitive than bronchial cells. All PM samples from Brescia inhibited intercellular communication mediated by gap junctions (GJIC), increased the total content in glutathione, and decreased the reduced form of glutathione, whereas the Reactive Oxygen Species (ROS) content was almost constant. Long-term treatments at higher doses of PM decreased MMP2 and MMP9 activity. Taken together, the results confirmed that PM is cytotoxic and can potentially act as tumour promoters, but the mechanisms involved in oxidative stress and lung homeostasis are dose- and time-dependent and quite complex. Full article
(This article belongs to the Special Issue The Influence of Environmental Factors on Disease and Health Outcomes)
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24 pages, 3272 KB  
Article
Environmental Temperature Variation Affects Brain Lipid Composition in Adult Zebrafish (Danio rerio)
by Elisa Maffioli, Simona Nonnis, Armando Negri, Manuela Fontana, Flavia Frabetti, Anna Rita Rossi, Gabriella Tedeschi and Mattia Toni
Int. J. Mol. Sci. 2024, 25(17), 9629; https://doi.org/10.3390/ijms25179629 - 5 Sep 2024
Cited by 3 | Viewed by 1915
Abstract
This study delves deeper into the impact of environmental temperature variations on the nervous system in teleost fish. Previous research has demonstrated that exposing adult zebrafish (Danio rerio) to 18 °C and 34 °C for 4 or 21 days induces behavioural [...] Read more.
This study delves deeper into the impact of environmental temperature variations on the nervous system in teleost fish. Previous research has demonstrated that exposing adult zebrafish (Danio rerio) to 18 °C and 34 °C for 4 or 21 days induces behavioural changes compared to fish kept at a control temperature of 26 °C, suggesting alterations in the nervous system. Subsequent studies revealed that these temperature conditions also modify brain protein expression, indicating potential neurotoxic effects. The primary aim of this work was to investigate the effects of prolonged exposure (21 days) to 18 °C or 34 °C on the brain lipidomes of adult zebrafish compared to a control temperature. Analysis of the brain lipidome highlighted significant alteration in the relative abundances of specific lipid molecules at 18 °C and 34 °C, confirming distinct effects induced by both tested temperatures. Exposure to 18 °C resulted in an increase in levels of phospholipids, such as phosphatidylethanolamine, alongside a general reduction in levels of sphingolipids, including sphingomyelin. Conversely, exposure to 34 °C produced more pronounced effects, with increases in levels of phosphatidylethanolamine and those of various sphingolipids such as ceramide, gangliosides, and sphingomyelin, alongside a reduction in levels of ether phospholipids, including lysophosphatidylethanolamine ether, phosphatidylethanolamine ether, and phosphatidylglycerol ether, as well as levels of glycolipids like monogalactosyldiacylglycerol. These results, when integrated with existing proteomic and behavioural data, offer new insights into the effects of thermal variations on the nervous system in teleost fish. Specifically, our proteomic and lipidomic findings suggest that elevated temperatures may disrupt mitochondrial function, increase neuronal susceptibility to oxidative stress and cytotoxicity, alter axonal myelination, impair nerve impulse transmission, hinder synapse function and neurotransmitter release, and potentially lead to increased neuronal death. These findings are particularly relevant in the fields of cell biology, neurobiology, and ecotoxicology, especially in the context of global warming. Full article
(This article belongs to the Special Issue The Influence of Environmental Factors on Disease and Health Outcomes)
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13 pages, 2592 KB  
Article
Synergistic Toxicity of Pollutant and Ultraviolet Exposure from a Mitochondrial Perspective
by Eloïse Larnac, Sébastien Méthot, Frédéric Pelchat, Marc-Antoine Millette, Alicia Montoni, Christian Salesse, Valérie Haydont, Laurent Marrot and Patrick J. Rochette
Int. J. Mol. Sci. 2024, 25(17), 9146; https://doi.org/10.3390/ijms25179146 - 23 Aug 2024
Cited by 1 | Viewed by 1472
Abstract
Ultraviolet (UV) exposure and atmospheric pollution are both independently implicated in skin diseases such as cancer and premature aging. UVA wavelengths, which penetrate in the deep layers of the skin dermis, exert their toxicity mainly through chromophore photosensitization reactions. Benzo[a]pyrene (BaP), the most [...] Read more.
Ultraviolet (UV) exposure and atmospheric pollution are both independently implicated in skin diseases such as cancer and premature aging. UVA wavelengths, which penetrate in the deep layers of the skin dermis, exert their toxicity mainly through chromophore photosensitization reactions. Benzo[a]pyrene (BaP), the most abundant polycyclic aromatic hydrocarbon originating from the incomplete combustion of organic matter, could act as a chromophore and absorb UVA. We and other groups have previously shown that BaP and UVA synergize their toxicity in skin cells, which leads to important oxidation. Even if mitochondria alterations have been related to premature skin aging and other skin disorders, no studies have focused on the synergy between UV exposure and pollution on mitochondria. Our study aims to investigate the combined effect of UVA and BaP specifically on mitochondria in order to assess the effect on mitochondrial membranes and the consequences on mitochondrial activity. We show that BaP has a strong affinity for mitochondria and that this affinity leads to an important induction of lipid peroxidation and membrane disruption when exposed to UVA. Co-exposure to UVA and BaP synergizes their toxicity to negatively impact mitochondrial membrane potential, mitochondrial metabolism and the mitochondrial network. Altogether, our results highlight the implication of mitochondria in the synergistic toxicity of pollution and UV exposure and the potential of this toxicity on skin integrity. Full article
(This article belongs to the Special Issue The Influence of Environmental Factors on Disease and Health Outcomes)
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