ArticleBiology of reproduction2016
Absence of Peroxiredoxin 6 Amplifies the Effect of Oxidant Stress on Mobility and SCSA/CMA3 Defined Chromatin Quality and Impairs Fertilizing Ability of Mouse Spermatozoa.
Article in Biology of reproduction, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 69 citations in OpenAlex.
- Molecular Advances in Male Infertility and Fertility: Importance of Redox Regulation and Oxidative Stress.International journal of molecular sciences · 2026Review
- HMG-CoA reductase inhibition preserves testicular function after torsion/detorsion by modulating oxidative stress and AKT signaling.Scientific reports · 2025Article
- Redox signaling regulation in human spermatozoa: a primary role of peroxiredoxins.Asian journal of andrology · 2025Review
- Role of Redox-Induced Protein Modifications in Spermatozoa in Health and Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Redox Regulation and Glucose Metabolism in the Stallion Spermatozoa.Antioxidants (Basel, Switzerland) · 2025Review
- The mechanism of oxidative stress in asthenozoospermia and antioxidant strategies: a review.Frontiers in endocrinology · 2025Review
- Essential role of germ cell glycerol-3-phosphate phosphatase for sperm health, oxidative stress control and male fertility in mice.Molecular metabolism · 2024Article
- LanCL2 Implicates in Testicular Redox Homeostasis and Acrosomal Maturation.Antioxidants (Basel, Switzerland) · 2024Article
- Peroxiredoxin 6 Peroxidase and CaAntioxidants (Basel, Switzerland) · 2022Article
- Mitochondrial Functionality in Male Fertility: From Spermatogenesis to Fertilization.Antioxidants (Basel, Switzerland) · 2021Review
- Testis-specific peroxiredoxin 4 variant is not absolutely required for spermatogenesis and fertility in mice.Scientific reports · 2020Article
- Relationship of Seminal Oxidation-Reduction Potential with Sperm DNA Integrity and pH in Idiopathic Infertile Patients.Biology · 2020Article
- A Novel Combination of γ-Tocopherol-Rich Mixture of Tocopherols and Ascorbic Acid Restores Fertility in Cases of Tyrosine Nitration-Associated Male Infertility in Mice.Antioxidants (Basel, Switzerland) · 2020Article
- Reactive Oxygen Species and Male Fertility.Antioxidants (Basel, Switzerland) · 2020Article
- Knockout Mouse Models for Peroxiredoxins.Antioxidants (Basel, Switzerland) · 2020Review
- Long-Term Adverse Effects of Oxidative Stress on Rat Epididymis and Spermatozoa.Antioxidants (Basel, Switzerland) · 2020Article
- Protective Role of Peroxiredoxins against Reactive Oxygen Species in Neonatal Rat Testicular Gonocytes.Antioxidants (Basel, Switzerland) · 2019Article
- Redox Regulation and Oxidative Stress: The Particular Case of the Stallion Spermatozoa.Antioxidants (Basel, Switzerland) · 2019Review
- Mouse Models of Genetically Altered Peroxiredoxin 6.Antioxidants (Basel, Switzerland) · 2019Review
- Peroxiredoxin 6: The Protector of Male Fertility.Antioxidants (Basel, Switzerland) · 2018Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Oxidative stress, the imbalance between reactive oxygen species production and antioxidant defenses, is associated with male infertility. Peroxiredoxins (PRDXs) are antioxidant enzymes with a wide distribution in spermatozoa. PRDX6 is highly abundant and located in all subcellular compartments of the spermatozoon. Infertile men have lower levels of sperm PRDX6 associated with low sperm motility and high DNA damage. In order to better understand the role of PRDX6 in male reproduction, the aim of this study was to elucidate the impact of the lack of PRDX6 on male mouse fertility. Spermatozoa lacking PRDX6 showed significantly increased levels of cellular oxidative damage evidenced by high levels of lipid peroxidation, 8-hydroxy-deoxyguanosine (DNA oxidation), and protein oxidation (S-glutathionylation and carbonylation), lower sperm chromatin quality (high DNA fragmentation and low DNA compaction, due to low levels of protamination and a high percentage of free thiols), along with decreased sperm motility and impairment of capacitation as compared with wild-type (WT) spermatozoa. These manifestations of damage are exacerbated by tert-butyl hydroperoxide treatment in vivo. While WT males partially recovered the quality of their spermatozoa (in terms of motility and sperm DNA integrity), Prdx6(-/-) males showed higher levels of sperm damage (lower motility and chromatin integrity) 6 mo after the end of treatment. In conclusion, Prdx6(-/-) males are more vulnerable to oxidative stress than WT males, resulting in impairment of sperm quality and ability to fertilize the oocyte, compatible with the subfertility phenotype observed in these knockout mice.
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Registered trials
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