Oxidative Stress and Male Reproductive Health—2nd Edition

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: 31 July 2026 | Viewed by 1462

Special Issue Editors


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Guest Editor
School of Environmental and Life Sciences, College of Engineering, Science and Environmental Science, University of Newcastle, Callaghan, NSW 2308, Australia
Interests: oxidative stress; antioxidants; reproductive biology; fertilization; demography
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Guest Editor
GReD Laboratory, Université Clermont Auvergne, CNRS UMR6293, INSERM U1103, Bâtiment CRBC, 28, Place Henri Dunant, 63000 Clermont-Ferrand, France
Interests: oxidative stress and male reproductive impacts; antioxidant therapy in male fertility; oxidative DNA damage
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress is a key factor in the aetiology of male infertility and is heavily involved in mediating the multiple impacts of age, lifestyle and environment on male reproductive function. In vitro, iatrogenic processes such as cryopreservation or prolonged incubation in media that have not been effectively engineered to reduce oxidative stress can also impact the functional and genetic integrity of human spermatozoa. Given the overwhelming importance of oxidative stress as a determinant of male reproductive health, there should be a role for antioxidant therapy in the treatment of this condition. However, much more research needs to be undertaken to determine the particular antioxidants to use, the circumstances under which they should they be administered and the precautions that should be taken to avoid reductive stress before this potential is realised.

This Special Issue aims to present a collection of high-quality papers describing the current status of research into oxidative stress and male reproductive health. It seeks to build on the success of the first volume in this series in deepening our understanding of this pathophysiological process and provide important insights into the current directions this rapidly moving field is taking.

As Guest Editor, I would like to invite you to contribute to this Special Issue on “Oxidative Stress and Male Reproductive Health—2nd Edition”. Original research reports and reviews will be published online in Antioxidants.

Prof. Dr. Robert John Aitken
Prof. Dr. Joel R. Drevet
Guest Editors

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Keywords

  • oxidative stress
  • antioxidant therapy
  • male reproductive health
  • male fertility
  • erectile dysfunction
  • prostatic disease
  • male ageing

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Published Papers (2 papers)

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Research

22 pages, 3296 KB  
Article
Levels of Protein CoAlation Regulate Redox Signaling Events of Human Sperm Capacitation
by Chika Onochie, Valeriy Filonenko, Ivan Gout and Cristian O’Flaherty
Antioxidants 2026, 15(5), 600; https://doi.org/10.3390/antiox15050600 - 9 May 2026
Viewed by 263
Abstract
Infertility is a global health problem, with male factors contributing to nearly half of all cases. Up to 30% of male infertility is classified as idiopathic, in part because routine semen analysis does not assess sperm fertilizing competence. Capacitation is a complex process [...] Read more.
Infertility is a global health problem, with male factors contributing to nearly half of all cases. Up to 30% of male infertility is classified as idiopathic, in part because routine semen analysis does not assess sperm fertilizing competence. Capacitation is a complex process that endows spermatozoa with the competence to fertilize the oocyte, and it depends on oxidant-driven phosphorylation events. These events include increased PKA substrate and tyrosine phosphorylation, which promote hyperactivated motility and the acrosome reaction. These pathways are normally restrained by decapacitation factors that must be relieved in the female reproductive tract before capacitation can proceed. Protein CoAlation is an antioxidant modification of protein thiols through a disulfide bond with coenzyme A (CoASH). We previously detected protein CoAlation in human spermatozoa and observed that its levels decline during capacitation, but its function was unknown. We hypothesized that protein CoAlation functions as a decapacitation mechanism that prevents redox signalling, enabling oxidative activation of phosphorylation events during capacitation. Using spermatozoa from healthy human donors, we leveraged subcellular fractionation, immunocytochemistry, computer-assisted sperm analysis (CASA), and immunoblotting to determine the sperm protein CoAlation profile, assess CoASH biosynthetic enzymes, and test how pharmacological modulation of CoAlation levels influences capacitation. CoAlated proteins were distributed across intracellular sperm compartments, and spermatozoa possess the CoASH biosynthetic enzymes PANK2 and CoASY, indicating an intrinsic capacity for CoAlation. Inhibition of CoASH biosynthesis reduced CoAlation and enhanced PKA substrate phosphorylation, tyrosine phosphorylation, hyperactivated motility, and the progesterone-induced acrosome reaction under capacitating conditions. Pantothenic acid supplementation increased CoAlation and suppressed these processes without impairing viability or baseline motility. These findings indicate that high levels of protein CoAlation in several protein bands are a pre-existing feature of the non-capacitated state that restrains the redox-regulated events of capacitation and that its decline is required to permit sperm capacitation. CoAlation levels may emerge as a biomarker of sperm capacitation and fertilizing competence. Full article
(This article belongs to the Special Issue Oxidative Stress and Male Reproductive Health—2nd Edition)
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15 pages, 6470 KB  
Article
Oxidative Damage, Antioxidant Capacity, and Apoptotic Activation in Varicocele: Biochemical Evidence of Improvement After Surgical Repair
by Erdem Orman, Hakki Uzun, Merve Huner Yigit, Ertugrul Yigit, Huseyin Cinar Zihni and Gorkem Akca
Antioxidants 2026, 15(4), 455; https://doi.org/10.3390/antiox15040455 - 5 Apr 2026
Viewed by 811
Abstract
To evaluate seminal oxidative stress, antioxidant defense, apoptosis-related activity, and Sertoli cell biomarkers in infertile men with grade 3 varicocele versus normozoospermic controls, and to assess postoperative changes after varicocelectomy. This prospective observational case–control study included 39 infertile men with grade 3 clinical [...] Read more.
To evaluate seminal oxidative stress, antioxidant defense, apoptosis-related activity, and Sertoli cell biomarkers in infertile men with grade 3 varicocele versus normozoospermic controls, and to assess postoperative changes after varicocelectomy. This prospective observational case–control study included 39 infertile men with grade 3 clinical varicocele and 44 normozoospermic controls. Seminal plasma levels of Malondialdehyde (MDA), 8-hydroxy-2′-deoxyguanosine (8-OHdG), superoxide dismutase (SOD), glutathione peroxidase-1 (GPx-1), reduced glutathione (GSH), nuclear factor erythroid 2–related factor 2 (NRF2), Kelch-like ECH-associated protein 1 (KEAP1), caspase-3, anti-Müllerian hormone (AMH), and inhibin B were measured by ELISA. Testicular volume, semen parameters, and diagnostic performance were also evaluated. Compared with controls, patients with varicocele had lower testicular volumes and impaired semen parameters. Seminal 8-OHdG and caspase-3 levels were higher, whereas SOD and inhibin B levels were lower. Baseline MDA, GPx-1, GSH, NRF2, KEAP1, and AMH levels did not differ significantly. After varicocelectomy, sperm concentration, total sperm count, progressive and total motility, total motile sperm count, morphology, and round cell count improved significantly. Postoperatively, caspase-3, MDA, and KEAP1 decreased, whereas SOD, GPx-1, GSH, NRF2, and inhibin B increased significantly. 8-OHdG showed a borderline decrease, and AMH remained unchanged. SOD showed the best diagnostic performance. Grade 3 varicocele is associated with oxidative DNA damage, impaired antioxidant defense, increased apoptotic signaling, and altered Sertoli cell-related seminal biomarkers. Varicocelectomy partially restores redox homeostasis, which may contribute to improved spermatogenic function. Full article
(This article belongs to the Special Issue Oxidative Stress and Male Reproductive Health—2nd Edition)
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