ArticleiScience2021
Secretory mouse quiescin sulfhydryl oxidase 1 aggregates defected human and mouse spermatozoa in vitro and in vivo.
Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed, 7 citations in OpenAlex.
- Seminal Vesicle-Derived Exosomes for the Regulation of Sperm Activity.Advances in anatomy, embryology, and cell biology · 2026Review
- Proteomic and functional analysis of alpaca (Frontiers in veterinary science · 2025Article
- A Comparison of White and Yellow Seminal Plasma Phosphoproteomes Obtained from Turkey (International journal of molecular sciences · 2024Article
- Polarized epithelium-sperm co-culture system reveals stimulatory factors for the secretion of mouse epididymal quiescin sulfhydryl oxidase 1.The Journal of reproduction and development · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A flavin-dependent enzyme quiescin Q6 sulfhydryl oxidase 1 (QSOX1) catalyzes the oxidation of thiol groups into disulfide bonds. QSOX1 is prominently expressed in the seminal plasma. However, its role in male reproduction is elusive. Here, we purified the secreted form of QSOX1, i.e., QSOX1c, from mouse seminal vesicle secretions and revealed for the first time its function involved in sperm physiology. Exogenous addition of QSOX1c time-dependently promoted the in vitro aggregation of thiol-rich, oxidative stressed, and apoptotic mouse and human sperm cells. Also, in vivo aggregated sperm cells collected from mouse uterine and human ejaculates also showed high levels of QSOX1c, intracellular reactive oxygen species, annexin V, and free thiols. In summary, our studies demonstrated that QSOX1c could agglutinate spermatozoa susceptible to free radical attack and apoptosis. This characteristic may provide an opportunity to separate defective sperm cells and improve sperm quality before artificial insemination in humans and animals.
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Registered trials
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