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Peroxiredoxin activity is a major landmark of male fertility
Peroxiredoxins (PRDXs) are important antioxidant enzymes reported to have a role in sperm function and male fertility. However, how PRDXs affects male fertility remain fundamental unanswered questions. We therefore sought to investigate the role of these enzymes in sperm function and fertilisation....
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5719347/ https://www.ncbi.nlm.nih.gov/pubmed/29215052 http://dx.doi.org/10.1038/s41598-017-17488-7 |
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author | Ryu, Do-Yeal Kim, Ki-Uk Kwon, Woo-Sung Rahman, Md Saidur Khatun, Amena Pang, Myung-Geol |
author_facet | Ryu, Do-Yeal Kim, Ki-Uk Kwon, Woo-Sung Rahman, Md Saidur Khatun, Amena Pang, Myung-Geol |
author_sort | Ryu, Do-Yeal |
collection | PubMed |
description | Peroxiredoxins (PRDXs) are important antioxidant enzymes reported to have a role in sperm function and male fertility. However, how PRDXs affects male fertility remain fundamental unanswered questions. We therefore sought to investigate the role of these enzymes in sperm function and fertilisation. In this in vitro trial, mouse spermatozoa were incubated with different concentrations of conoidin A (1, 10, or 100 µM), a specific inhibitor of PRDXs. Our results demonstrated that inhibition of PRDXs by conoidin A significantly decreased the oxidized form of peroxiredoxins (PRDXs-SO(3)) in spermatozoa. Decreased PRDX activity was associated with a significant reduction in sperm motility parameters, viability, and intracellular ATP, whereas ROS levels, DNA fragmentation, and loss of mitochondrial membrane potential were increased. Simultaneously capacitation and the acrosome reaction were also significantly inhibited perhaps as a consequence of decreased tyrosine phosphorylation and protein kinase-A activity. In addition, fertilisation and early embryonic development were adversely affected following PRDXs inhibition in spermatozoa. Taken together, our data demonstrate that decreased PRDX activity directly affects male fertility due to negative effects on important functions and biochemical properties of spermatozoa, ultimately leading to poor fertilisation and embryonic development. |
format | Online Article Text |
id | pubmed-5719347 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-57193472017-12-08 Peroxiredoxin activity is a major landmark of male fertility Ryu, Do-Yeal Kim, Ki-Uk Kwon, Woo-Sung Rahman, Md Saidur Khatun, Amena Pang, Myung-Geol Sci Rep Article Peroxiredoxins (PRDXs) are important antioxidant enzymes reported to have a role in sperm function and male fertility. However, how PRDXs affects male fertility remain fundamental unanswered questions. We therefore sought to investigate the role of these enzymes in sperm function and fertilisation. In this in vitro trial, mouse spermatozoa were incubated with different concentrations of conoidin A (1, 10, or 100 µM), a specific inhibitor of PRDXs. Our results demonstrated that inhibition of PRDXs by conoidin A significantly decreased the oxidized form of peroxiredoxins (PRDXs-SO(3)) in spermatozoa. Decreased PRDX activity was associated with a significant reduction in sperm motility parameters, viability, and intracellular ATP, whereas ROS levels, DNA fragmentation, and loss of mitochondrial membrane potential were increased. Simultaneously capacitation and the acrosome reaction were also significantly inhibited perhaps as a consequence of decreased tyrosine phosphorylation and protein kinase-A activity. In addition, fertilisation and early embryonic development were adversely affected following PRDXs inhibition in spermatozoa. Taken together, our data demonstrate that decreased PRDX activity directly affects male fertility due to negative effects on important functions and biochemical properties of spermatozoa, ultimately leading to poor fertilisation and embryonic development. Nature Publishing Group UK 2017-12-07 /pmc/articles/PMC5719347/ /pubmed/29215052 http://dx.doi.org/10.1038/s41598-017-17488-7 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Ryu, Do-Yeal Kim, Ki-Uk Kwon, Woo-Sung Rahman, Md Saidur Khatun, Amena Pang, Myung-Geol Peroxiredoxin activity is a major landmark of male fertility |
title | Peroxiredoxin activity is a major landmark of male fertility |
title_full | Peroxiredoxin activity is a major landmark of male fertility |
title_fullStr | Peroxiredoxin activity is a major landmark of male fertility |
title_full_unstemmed | Peroxiredoxin activity is a major landmark of male fertility |
title_short | Peroxiredoxin activity is a major landmark of male fertility |
title_sort | peroxiredoxin activity is a major landmark of male fertility |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5719347/ https://www.ncbi.nlm.nih.gov/pubmed/29215052 http://dx.doi.org/10.1038/s41598-017-17488-7 |
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