Oxidative stress and male infertility.

antioxidants lipid peroxidation male infertility oxidative stress reactive oxygen species

Journal

Reproductive medicine and biology
ISSN: 1445-5781
Titre abrégé: Reprod Med Biol
Pays: Japan
ID NLM: 101213278

Informations de publication

Date de publication:
Jan 2021
Historique:
received: 18 04 2020
revised: 19 09 2020
accepted: 28 09 2020
entrez: 25 1 2021
pubmed: 26 1 2021
medline: 26 1 2021
Statut: epublish

Résumé

Between 30% and 80% of patients with male infertility produce excessive reactive oxygen species (ROS) in their ejaculate even though the cause of male infertility is unexplained in approximately half of cases. The strong connection between oxidative stress (OS) and male infertility has led recent investigators to propose the term "Male Oxidative Stress Infertility (MOSI)" to describe OS-associated male infertility. We searched the PubMed database for original and review articles to survey the effects of OS on male infertility, and then verified the effects and treatments. Seminal plasma contains many antioxidants that protect sperm from ROS, because low amounts of ROS are required in the physiological fertilization process. The production of excessive ROS causes OS which can lower fertility through lipid peroxidation, sperm DNA damage, and apoptosis. Several assays are available for evaluating OS, including the MiOXSYS® analyzer to measure oxidation-reduction potential. Several measures should be considered for minimizing OS and improving clinical outcomes. Accurately diagnosing patients with MOSI and identifying highly sensitive biomarkers through proteomics technology is vital for better clinical outcomes.

Sections du résumé

BACKGROUND BACKGROUND
Between 30% and 80% of patients with male infertility produce excessive reactive oxygen species (ROS) in their ejaculate even though the cause of male infertility is unexplained in approximately half of cases. The strong connection between oxidative stress (OS) and male infertility has led recent investigators to propose the term "Male Oxidative Stress Infertility (MOSI)" to describe OS-associated male infertility.
METHODS METHODS
We searched the PubMed database for original and review articles to survey the effects of OS on male infertility, and then verified the effects and treatments.
MAIN FINDINGS RESULTS
Seminal plasma contains many antioxidants that protect sperm from ROS, because low amounts of ROS are required in the physiological fertilization process. The production of excessive ROS causes OS which can lower fertility through lipid peroxidation, sperm DNA damage, and apoptosis. Several assays are available for evaluating OS, including the MiOXSYS® analyzer to measure oxidation-reduction potential. Several measures should be considered for minimizing OS and improving clinical outcomes.
CONCLUSION CONCLUSIONS
Accurately diagnosing patients with MOSI and identifying highly sensitive biomarkers through proteomics technology is vital for better clinical outcomes.

Identifiants

pubmed: 33488282
doi: 10.1002/rmb2.12353
pii: RMB212353
pmc: PMC7812476
doi:

Types de publication

Journal Article Review

Langues

eng

Pagination

41-52

Informations de copyright

© 2020 The Authors. Reproductive Medicine and Biology published by John Wiley & Sons Australia, Ltd on behalf of Japan Society for Reproductive Medicine.

Déclaration de conflit d'intérêts

Conflicts of interest: The authors report no declarations of interest. Human/animal rights statements and informed consent: This article does not contain any studies with human and animal subjects performed by any of the authors. Approval by Ethics Committee: This research was supported by the Ethics Committee of Yokohama City University Medical Center.

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Auteurs

Teppei Takeshima (T)

Department of Urology, Reproduction Center Yokohama City University Medical Center Yokohama city Japan.

Kimitsugu Usui (K)

Department of Urology, Reproduction Center Yokohama City University Medical Center Yokohama city Japan.

Kohei Mori (K)

Department of Urology, Reproduction Center Yokohama City University Medical Center Yokohama city Japan.

Takuo Asai (T)

Department of Urology, Reproduction Center Yokohama City University Medical Center Yokohama city Japan.

Kengo Yasuda (K)

Department of Urology, Reproduction Center Yokohama City University Medical Center Yokohama city Japan.

Shinnosuke Kuroda (S)

Department of Urology, Reproduction Center Yokohama City University Medical Center Yokohama city Japan.

Yasushi Yumura (Y)

Department of Urology, Reproduction Center Yokohama City University Medical Center Yokohama city Japan.

Classifications MeSH