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Biology
Special Issues
Advances in Redox Metabolism and Cellular Homeostasis
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Advances in Redox Metabolism and Cellular Homeostasis

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Biochemistry and Molecular Biology".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 620

Special Issue Editors

Dr. Alexios Vlamis-Gardikas

E-Mail Website
Guest Editor
Department of Chemistry, University of Patras, 26504 Rion, Greece
Interests: thioredoxins; glutaredoxins; thioredoxin reductase; toxins/antitoxins; antimicrobials
Special Issues, Collections and Topics in MDPI journals
Dr. Jianqiang Xu

E-Mail Website
Guest Editor
School of Chemical Enginnering, Ocean Technology and Life Science (CEOTLS), Dalian University of Technology, Panjin 124221, China
Interests: thioredoxin reductase; selenoprotein; inflammation; tumor drug resistance; small molecule inhibitor; ferroptosis; oxidative stress; disulfide stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cells require well-defined and strictly regulated redox environments to maintain their normal metabolism. Although this may sound somewhat static, it is not; cells live in dynamic states according to their surrounding environments and their current or destined states of differentiation. While living cells are intrinsically dependent on systems of electron flow to produce ATP for their energy needs, the physicochemical conditions that maintain the electron flow ensure that cells live under continuous oxidative stress. The desired/undesired electron flow and all mechanisms to reverse it in living cells are the cores of biology, and they have fascinated scientists for years.

We are pleased to invite you to submit to this Special Issue, entitled “Advances in Redox Metabolism and Cellular Homeostasis”. This Special Issue aims to present novel findings related to normal cellular life and adaptations in responses to different kinds of stress, all ultimately related to redox biology.

In this Special Issue, original research articles and reviews are welcome to be submitted. Research areas may include, but are not limited to, all kinds of cells and organisms, all enzymatic systems participating in normal metabolism or antioxidant mechanisms, and, of course, all modifications of individual molecules to achieve these aims.

We look forward to receiving your contributions.

Dr. Alexios Vlamis-Gardikas
Dr. Jianqiang Xu
Guest Editors

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. Biology 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 2700 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

  • oxidative stress
  • peroxiredoxins
  • hydrogen peroxide
  • redox regulation
  • thiol modification
  • reactive oxygen species
  • iron sulfur clusters
  • redox signaling

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Published Papers (1 paper)

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Research

13 pages, 1948 KiB  
Article
Chronic Variable Stress May Induce Apoptosis in the Testis and Epididymal Sperm of Young Male Rats
by Yeimy Mar De León-Ramírez, Leticia Nicolás-Toledo, Eliut Pérez-Sánchez and Omar Arroyo-Helguera
Biology 2025, 14(6), 690; https://doi.org/10.3390/biology14060690 - 12 Jun 2025
Viewed by 398
Abstract
Stressor stimuli induce oxidative stress and functional abnormalities in sperm, which are linked to a reduced sperm quality and male infertility. Furthermore, oxidative stress can trigger cell death. However, the impact of stressor stimulation on testicles and epididymal sperms and apoptosis has not [...] Read more.
Stressor stimuli induce oxidative stress and functional abnormalities in sperm, which are linked to a reduced sperm quality and male infertility. Furthermore, oxidative stress can trigger cell death. However, the impact of stressor stimulation on testicles and epididymal sperms and apoptosis has not been explored. This study analyzes the expression of extrinsic and intrinsic apoptotic markers in the testicle and epididymis of rats exposed to chronic variable stress (CVS). We used male Wistar rats divided into two groups: the control group was kept undisrupted, and the stress group was stressed daily using a CVS model for four weeks, except for the weekends (from postnatal days 51 to 81). After the last week, the rats were sacrificed, and complete testicles and epididymal sperm were used to measure oxidative stress and the total antioxidant status by colorimetric methods. The expressions of PPAR-γ, p53, Bax, and Bcl-2 markers at the mRNA level were determined by real-time PCR, and the p-Akt, AP-2α, PPAR-γ, C/EBP-β and FAS protein levels were detected by immunoblot. The results showed low levels of p-Akt and AP-2α proteins and high levels of FAS, PPAR-γ, and C/EBP-β in the testicle and epididymis of rats exposed to CVS. At the mRNA level, we observed the upregulation of PPAR-γ, p53, p21, HIF-α, and Bax expressions in the epididymis of rats exposed to CVS, consistent with the significant caspase-3 activity observed in both the epididymis and testicles in the CVS group. In conclusion, CVS damage triggers the induction of apoptosis markers by intrinsic (PPAR-γ, p53, p21, HIF-α, and Bax) and extrinsic (p-Akt, AP-2α, and FAS) caspase-3-dependent pathways in complete extracts of both the testicles and epididymis. This study supports the view that stressor stimuli could be involved in the infertility process. Full article
(This article belongs to the Special Issue Advances in Redox Metabolism and Cellular Homeostasis)
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