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Antioxidants
Special Issues
Redox Response under Social and Chemical Stress
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Redox Response under Social and Chemical 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: 10 November 2024 | Viewed by 1003

Special Issue Editor

Prof. Dr. Rosita Gabbianelli

E-Mail Website
Guest Editor
School of Pharmacy, University of Camerino, Camerino (MC), Italy
Interests: epigenetics and neurodegeneration; nutrigenomics; xenobiotics and redox system
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

"Redox Response under Social and Chemical Stress" is a research topic that focuses on how organisms respond to stressors in their environment, both social and chemical, by altering their redox signaling pathways. Redox signaling is the process by which cells communicate with each other through the transfer of electrons, and it plays a critical role in many cellular processes, including stress responses. 

The study of redox response under stress is important because stress can have a significant impact on the health and well-being of organisms and understanding the mechanisms by which organisms respond to stress can help to identify potential therapeutic targets for stress-related diseases. Social stress, such as that experienced by animals in social hierarchies, has been shown to have a negative impact on cellular redox balance, while exposure to chemical stressors, such as pollutants or drugs, can also cause oxidative stress and disrupt redox signaling pathways.

The capacity to respond to stressors can vary across one’s life, and the exposure to subliminal factors has a critical impact during early life compared to the same experience at the adult age. Early phycological stressors (i.e., childhood trauma) or exposure to chemicals (i.e. pesticides, endocrine disruptors) during early life have been associated with an increased risk for age-related disorders. 

This Special Issue aims to publish original research papers, systematic reviews and meta-analyses that contribute to a better understand of the ability of organisms to cope with stress and develop strategies to mitigate the negative effects of stress on health and well-being.

Prof. Dr. Rosita Gabbianelli
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

  • redox balance
  • redox signaling
  • exposome
  • social stress
  • chemical stress
  • oxidative stress

Published Papers (1 paper)

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Research

22 pages, 2762 KiB  
Article
Influence of Mild Chronic Stress and Social Isolation on Acute Ozone-Induced Alterations in Stress Biomarkers and Brain-Region-Specific Gene Expression in Male Wistar–Kyoto Rats
by Matthew C. Valdez, Danielle L. Freeborn, Joseph M. Valdez, Andres R. Henriquez, Samantha J. Snow, Thomas W. Jackson, Prasada Rao S. Kodavanti and Urmila P. Kodavanti
Antioxidants 2023, 12(11), 1964; https://doi.org/10.3390/antiox12111964 - 03 Nov 2023
Viewed by 802
Abstract
Individuals with psychosocial stress often experience an exaggerated response to air pollutants. Ozone (O3) exposure has been associated with the activation of the neuroendocrine stress-response system. We hypothesized that preexistent mild chronic stress plus social isolation (CS), or social isolation (SI) [...] Read more.
Individuals with psychosocial stress often experience an exaggerated response to air pollutants. Ozone (O3) exposure has been associated with the activation of the neuroendocrine stress-response system. We hypothesized that preexistent mild chronic stress plus social isolation (CS), or social isolation (SI) alone, would exacerbate the acute effects of O3 exposure on the circulating adrenal-derived stress hormones, and the expression of the genes regulating glucocorticoid stress signaling via an altered stress adaptation in a brain-region-specific manner. Male Wistar–Kyoto rats (5 weeks old) were socially isolated, plus were subjected to either CS (noise, confinement, fear, uncomfortable living, hectic activity, and single housing), SI (single housing only, restricted handling and no enrichment) or no stress (NS; double housing, frequent handling and enrichment provided) for 8 weeks. The rats were then exposed to either air or O3 (0.8 ppm for 4 h), and the samples were collected immediately after. The indicators of sympathetic and hypothalamic–pituitary axis (HPA) activation (i.e., epinephrine, corticosterone, and lymphopenia) increased with O3 exposure, but there were no effects from CS or SI, except for the depletion of serum BDNF. CS and SI revealed small changes in brain-region-specific glucocorticoid-signaling-associated markers of gene expression in the air-exposed rats (hypothalamic Nr3c1, Nr3c2 Hsp90aa1, Hspa4 and Cnr1 inhibition in SI; hippocampal HSP90aa1 increase in SI; and inhibition of the bed nucleus of the stria terminalis (BNST) Cnr1 in CS). Gene expression across all brain regions was altered by O3, reflective of glucocorticoid signaling effects, such as Fkbp5 in NS, CS and SI. The SI effects on Fkbp5 were greatest for SI in BNST. O3 increased Cnr2 expression in the hypothalamus and olfactory bulbs of the NS and SI groups. O3, in all stress conditions, generally inhibited the expression of Nr3c1 in all brain regions, Nr3c2 in the hippocampus and hypothalamus and Bdnf in the hippocampus. SI, in general, showed slightly greater O3-induced changes when compared to NS and CS. Serum metabolomics revealed increased sphingomyelins in the air-exposed SI and O3-exposed NS, with underlying SI dampening some of the O3-induced changes. These results suggest a potential link between preexistent SI and acute O3-induced increases in the circulating adrenal-derived stress hormones and brain-region-specific gene expression changes in glucocorticoid signaling, which may partly underlie the stress dynamic in those with long-term SI. Full article
(This article belongs to the Special Issue Redox Response under Social and Chemical Stress)
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