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Antioxidants
Special Issues
Environmental Pollution and Oxidative Stress
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Environmental Pollution and Oxidative Stress

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 20 October 2024 | Viewed by 3727

Special Issue Editor

Prof. Dr. Selva Rivas-Arancibia

E-Mail Website
Guest Editor
Laboratory of Oxidative Stress and Brain Plasticity, Department of Physiology, School of Medicine, National Autonomous University of Mexico, Coyoacan, Mexico City 04510, Mexico
Interests: environmental pollution; oxidative stress; inflammatory response; immune response; regulatory T cells; epigenetic; degenerative diseases; autoimmune diseases; antioxidants

Special Issue Information

Dear Colleagues,

The effect of environmental pollution on the population is a severe public health problem, mainly in highly populated cities and highly industrialized places. Repeated exposure to environmental pollutants, such as ozone and suspended particles, is directly associated with non-infectious chronic degenerative diseases, as well as with their progression. There are multiple ways by which environmental pollution is associated with degenerative diseases. However, it is demonstrated that air pollution by ozone or suspended particles causes oxidative stress and a chronic inflammatory response that has lost its regulation. Considering the role of oxidative signals in cell evolution and their role in the homeostasis of physiological functions, we can understand why chronic alterations in redox signaling lead to impaired signaling in both cells and the organism. These cause a vicious circle between the state of oxidative stress and the loss of regulation of the inflammatory response in degenerative diseases since, once the degenerative process is triggered, it is not possible to reverse it. Therefore, ozone contaminations and suspended particles are associated with autoimmune, cardiovascular diseases, heart attacks, strokes, cancer, degenerative and neurodegenerative diseases, etc.

Prof. Dr. Selva Rivas-Arancibia
Guest Editor

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. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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

  • environmental pollution
  • oxidative stress
  • inflammatory response
  • immune response
  • regulatory T cells
  • epigenetic
  • degenerative diseases
  • autoimmune diseases
  • antioxidants

Published Papers (3 papers)

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Research

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19 pages, 7535 KiB  
Article
Protective Effects of Isoliquiritigenin and Licochalcone B on the Immunotoxicity of BDE-47: Antioxidant Effects Based on the Activation of the Nrf2 Pathway and Inhibition of the NF-κB Pathway
by Minghui Dong, Ziying Yang, Qian Gao, Qingyuan Deng, Le Li and Hongmei Chen
Antioxidants 2024, 13(4), 445; https://doi.org/10.3390/antiox13040445 - 10 Apr 2024
Viewed by 511
Abstract
2,2′,4,4′-Tetrabrominated biphenyl ether (BDE-47) is a polybrominated diphenyl ether (PBDE) homologue that is ubiquitous in biological samples and highly toxic to humans and other organisms. Prior research has confirmed that BDE-47 can induce oxidative damage in RAW264.7 cells, resulting in apoptosis and impaired [...] Read more.
2,2′,4,4′-Tetrabrominated biphenyl ether (BDE-47) is a polybrominated diphenyl ether (PBDE) homologue that is ubiquitous in biological samples and highly toxic to humans and other organisms. Prior research has confirmed that BDE-47 can induce oxidative damage in RAW264.7 cells, resulting in apoptosis and impaired immune function. The current study mainly focused on how Isoliquiritigenin (ISL) and Licochalcone B (LCB) might protect against BDE-47’s immunotoxic effects on RAW264.7 cells. The results show that ISL and LCB could increase phagocytosis, increase the production of MHC-II, and decrease the production of inflammatory factors (TNF-α, IL-6, and IL-1β) and co-stimulatory factors (CD40, CD80, and CD86), alleviating the immune function impairment caused by BDE-47. Secondly, both ISL and LCB could reduce the expressions of the proteins Bax and Caspase-3, promote the expression of the protein Bcl-2, and reduce the apoptotic rate, alleviating the apoptosis initiated by BDE-47. Additionally, ISL and LCB could increase the levels of antioxidant substances (SOD, CAT, and GSH) and decrease the production of reactive oxygen species (ROS), thereby counteracting the oxidative stress induced by BDE-47. Ultimately, ISL and LCB suppress the NF-κB pathway by down-regulating IKBKB and up-regulating IκB-Alpha in addition to activating the Nrf2 pathway and promoting the production of HO-1 and NQO1. To summarize, BDE-47 causes oxidative damage that can be mitigated by ISL and LCB through the activation of the Nrf2 pathway and inhibition of the NF-κB pathway, which in turn prevents immune function impairment and apoptosis. These findings enrich the current understanding of the toxicological molecular mechanism of BDE-47 and the detoxification mechanism of licorice. Full article
(This article belongs to the Special Issue Environmental Pollution and Oxidative Stress)
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Review

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17 pages, 2487 KiB  
Review
Light Pollution and Oxidative Stress: Effects on Retina and Human Health
by Rocío Salceda
Antioxidants 2024, 13(3), 362; https://doi.org/10.3390/antiox13030362 - 18 Mar 2024
Viewed by 1060
Abstract
Visible light refers to the frequencies within the electromagnetic spectrum that humans can see, encompassing radiation with wavelengths falling between 380 nm to 760 nm. The energy of a single photon increases with its frequency. In the retina, photoreceptor cells contain light-sensitive pigments [...] Read more.
Visible light refers to the frequencies within the electromagnetic spectrum that humans can see, encompassing radiation with wavelengths falling between 380 nm to 760 nm. The energy of a single photon increases with its frequency. In the retina, photoreceptor cells contain light-sensitive pigments that absorb light and convert it into electrical stimuli through a process known as phototransduction. However, since the absorption spectrum of photoreceptors closely aligns with blue light (ranging from 400 to 500 nm), exposure to high light intensities or continuous illumination can result in oxidative stress within these cells, leading to a loss of their functionality. Apart from photoreceptor cells, the retina also houses photosensitive ganglion cells, known as intrinsically photosensitive retinal ganglion cells (ipRGCs). These cells relay information to the suprachiasmatic nucleus in the brain, playing a crucial role in modulating melatonin secretion, which in turn helps in synchronizing the body’s circadian rhythms and responses to seasonal changes. Both, ipRGCs and skin possess a peak sensitivity to blue wavelengths, rendering them particularly susceptible to the effects of excessive blue light exposure. This study delves into the consequences of excessive illumination and/or prolonged exposure to blue light on retinal function and explores its implications for human health. Full article
(This article belongs to the Special Issue Environmental Pollution and Oxidative Stress)
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14 pages, 2656 KiB  
Review
Ozone Environmental Pollution: Relationship between the Intestine and Neurodegenerative Diseases
by Selva Rivas-Arancibia, Alfredo Miranda-Martínez, Erika Rodríguez-Martínez, Eduardo Hernández-Orozco, Marlen Valdés-Fuentes and Roberto De la Rosa-Sierra
Antioxidants 2023, 12(7), 1323; https://doi.org/10.3390/antiox12071323 - 22 Jun 2023
Viewed by 1672
Abstract
Repeated exposure to environmental ozone causes a chronic state of oxidative stress. This state is present in chronic degenerative diseases and induces a loss of control of the inflammatory response. Redox system dysfunction and failures in control of inflammatory responses are involved in [...] Read more.
Repeated exposure to environmental ozone causes a chronic state of oxidative stress. This state is present in chronic degenerative diseases and induces a loss of control of the inflammatory response. Redox system dysfunction and failures in control of inflammatory responses are involved in a vicious circle that maintains and increases the degenerative process. The intestine also responds to secondary reactive species formed by exposure to ozone doses, generating noxious stimuli that increase degenerative damage. This review aims to elucidate how environmental pollution, mainly by ozone, induces a state of chronic oxidative stress with the loss of regulation of the inflammatory response, both in the intestine and in the brain, where the functionality of both structures is altered and plays a determining role in some neurodegenerative and chronic degenerative diseases. For this purpose, we searched for information on sites such as the Cochrane Library Database, PubMed, Scopus, and Medscape. Reviewing the data published, we can conclude that environmental pollutants are a severe health problem. Ozone pollution has different pathways of action, both molecular and systemic, and participates in neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease as well in bowel diseases as Inflammatory Bowel Disease, Crohn’s Disease, and Irritable Bowel Syndrome. Full article
(This article belongs to the Special Issue Environmental Pollution and Oxidative Stress)
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