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Review
. 2024 Apr 25;15(5):539.
doi: 10.3390/genes15050539.

Oxidative Stress Biomarkers in Male Infertility: Established Methodologies and Future Perspectives

Affiliations
Review

Oxidative Stress Biomarkers in Male Infertility: Established Methodologies and Future Perspectives

Filomena Mottola et al. Genes (Basel). .

Abstract

Male fertility can be affected by oxidative stress (OS), which occurs when an imbalance between the production of reactive oxygen species (ROS) and the body's ability to neutralize them arises. OS can damage cells and influence sperm production. High levels of lipid peroxidation have been linked to reduced sperm motility and decreased fertilization ability. This literature review discusses the most commonly used biomarkers to measure sperm damage caused by ROS, such as the high level of OS in seminal plasma as an indicator of imbalance in antioxidant activity. The investigated biomarkers include 8-hydroxy-2-deoxyguanosine acid (8-OHdG), a marker of DNA damage caused by ROS, and F2 isoprostanoids (8-isoprostanes) produced by lipid peroxidation. Furthermore, this review focuses on recent methodologies including the NGS polymorphisms and differentially expressed gene (DEG) analysis, as well as the epigenetic mechanisms linked to ROS during spermatogenesis along with new methodologies developed to evaluate OS biomarkers. Finally, this review addresses a valuable insight into the mechanisms of male infertility provided by these advances and how they have led to new treatment possibilities. Overall, the use of biomarkers to evaluate OS in male infertility has supplied innovative diagnostic and therapeutic approaches, enhancing our understanding of male infertility mechanisms.

Keywords: epigenetic alterations; infertility; omics; oxidative stress; sperm DNA damage.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
The main consequences of oxidative stress in sperm due to the formation of reactive oxygen species (ROS) and/or reduction of antioxidant enzyme activity.
Figure 2
Figure 2
Generation of ROS from sequential transfer of electrons from complete reduction to water.
Figure 3
Figure 3
Graphical illustration of epigenetic modifications. These can be divided into 4 classes: (I) DNA methylation, (II) histone modifications, (III) chromatin remodeling, and (IV) non-coding RNA regulation.

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References

    1. Du Plessis S.S., Agarwal A., Halabi J., Tvrda E. Contemporary evidence on the physiological role of reactive oxygen species in human sperm function. J. Assist. Reprod. Genet. 2015;32:509–520. doi: 10.1007/s10815-014-0425-7. - DOI - PMC - PubMed
    1. Bisht S., Dada R. Oxidative stress: Major executioner in disease pathology, role in sperm DNA damage and preventive strategies. Front. Biosci. (Schol. Ed.) 2017;9:420–447. doi: 10.2741/s495. - DOI - PubMed
    1. Mottola F., Iovine C., Carannante M., Santonastaso M., Rocco L. In Vitro Combination of Ascorbic and Ellagic Acids in Sperm Oxidative Damage Inhibition. Int. J. Mol. Sci. 2022;23:14751. doi: 10.3390/ijms232314751. - DOI - PMC - PubMed
    1. Finelli R., Mottola F., Agarwal A. Impact of Alcohol Consumption on Male Fertility Potential: A Narrative Review. Int. J. Environ. Res. Public Health. 2021;19:328. doi: 10.3390/ijerph19010328. - DOI - PMC - PubMed
    1. Fraga C.G., Motchnik P.A., Wyrobek A.J., Rempel D.M., Ames B.N. Smoking and low antioxidant levels increase oxidative damage to sperm DNA. Mutat. Res. 1996;351:199–203. doi: 10.1016/0027-5107(95)00251-0. - DOI - PubMed

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This research received no external funding.
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