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Effects of Environmental Contaminants on Cell Signaling Pathways

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

Deadline for manuscript submissions: 25 June 2024 | Viewed by 1036

Special Issue Editor


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Guest Editor
Department of Speech Communication, Oregon State University, Corvallis, OR 97331, USA
Interests: environmental health; toxicology; in vitro biology; signal transduction; cell communication; gap junctions; environmental toxicants

Special Issue Information

Dear Colleagues,

This Special Issue will focus on the effects of environmental contaminants on cell signaling pathways. The normal development of an organism begins at embryogenesis and continues through fetal, neonatal, and adolescent development, and the maintenance of adult tissues requires a delicate balance of a complex set of intra-, inter-, and extracellular-communication mechanisms controlling gene expression. The interruption of these cell communication systems by environmental contaminants results in growth and development pathologies. Within a tissue, cells typically function as communities, often termed syncytia, in which intercellular communication through gap junctions is pivotal in coordinating the intracellular signaling pathways controlling gene expression that maintains a balance between proliferation, differentiation, and apoptosis. Understanding the molecular basis by which environmental contaminants alter these pathways, particularly the central role gap junctions play in this process, will provide a more accurate mechanistic understanding of the pathologies of environmental toxicants.

Dr. Brad L. Upham
Guest Editor

Manuscript Submission Information

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Keywords

  • cell signaling
  • environmental contaminants
  • signal transduction
  • gap junction
  • toxic mechanisms

Published Papers (1 paper)

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Research

12 pages, 2601 KiB  
Article
Lipid Peroxidation as the Mechanism Underlying Polycyclic Aromatic Hydrocarbons and Sunlight Synergistic Toxicity in Dermal Fibroblasts
by Eloïse Larnac, Alicia Montoni, Valérie Haydont, Laurent Marrot and Patrick J. Rochette
Int. J. Mol. Sci. 2024, 25(3), 1905; https://doi.org/10.3390/ijms25031905 - 05 Feb 2024
Cited by 1 | Viewed by 786
Abstract
Light and atmospheric pollution are both independently implicated in cancer induction and premature aging. Evidence has been growing more recently on the toxic synergy between light and pollutants. Polycyclic aromatic hydrocarbons (PAHs) originate from the incomplete combustion of organic matter. Some PAHs, such [...] Read more.
Light and atmospheric pollution are both independently implicated in cancer induction and premature aging. Evidence has been growing more recently on the toxic synergy between light and pollutants. Polycyclic aromatic hydrocarbons (PAHs) originate from the incomplete combustion of organic matter. Some PAHs, such as the Benzo[a]pyrene (BaP), absorb ultraviolet A (UVA) wavelengths and can act as exogenous chromophores, leading to synergistic toxicity through DNA damage and cytotoxicity concomitant to ROS formation. In this study, we shed light on the mechanism underlying the toxic synergy between PAHs and UVA. Using dermal fibroblasts co-exposed to UVA and BaP, we have demonstrated that the photosensitization reaction causes mortality, which is most likely caused by ROS accumulation. We have shown that these ROS are concentrated in the lipids, which causes an important induction of lipid peroxidation and malondialdehyde, by-products of lipid peroxidation. We have also shown the accumulation of bulky DNA damage, most likely generated by these by-products of lipid peroxidation. To our knowledge, this study represents the first one depicting the molecular effects of photo-pollution on dermal skin. Full article
(This article belongs to the Special Issue Effects of Environmental Contaminants on Cell Signaling Pathways)
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