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Effect of antioxidants on BPA-induced stress on sperm function in a mouse model
In the past few years, bisphenol A, (BPA) an endocrine-disrupting chemical, has received increasing attention because of its detrimental health effects. There is ample evidence to support that BPA interferes with the reproductive health of humans and animals. In spermatozoa, BPA-induced adverse effe...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6646364/ https://www.ncbi.nlm.nih.gov/pubmed/31332285 http://dx.doi.org/10.1038/s41598-019-47158-9 |
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author | Rahman, Md Saidur Kang, Kyu-Ho Arifuzzaman, Sarder Pang, Won-Ki Ryu, Do-Yeal Song, Won-Hee Park, Yoo-Jin Pang, Myung-Geol |
author_facet | Rahman, Md Saidur Kang, Kyu-Ho Arifuzzaman, Sarder Pang, Won-Ki Ryu, Do-Yeal Song, Won-Hee Park, Yoo-Jin Pang, Myung-Geol |
author_sort | Rahman, Md Saidur |
collection | PubMed |
description | In the past few years, bisphenol A, (BPA) an endocrine-disrupting chemical, has received increasing attention because of its detrimental health effects. There is ample evidence to support that BPA interferes with the reproductive health of humans and animals. In spermatozoa, BPA-induced adverse effects are mostly caused by increased oxidative stress. Using an in vitro experimental model, we examined whether antioxidants (glutathione, vitamin C, and vitamin E) have defensive effects against BPA-induced stress in spermatozoa. The results showed that antioxidants inhibit the overproduction of reactive oxygen species (basically cellular peroxides) and increase intracellular ATP levels, thereby preventing motility loss and abnormal acrosome reaction in BPA-exposed spermatozoa. In particular, glutathione and vitamin E reduced the protein kinase A-dependent tyrosine phosphorylation in spermatozoa and, thus, prevented the precocious acrosome reaction from occurring. Furthermore, we found that the compromised fertilisation and early embryo development mediated by BPA-exposed spermatozoa can be improved following their supplementation with glutathione and vitamin E. Based on these findings, we suggest that antioxidants reduce oxidative stress in BPA-exposed spermatozoa, thus preventing detrimental effects on their function and fertility. |
format | Online Article Text |
id | pubmed-6646364 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-66463642019-07-29 Effect of antioxidants on BPA-induced stress on sperm function in a mouse model Rahman, Md Saidur Kang, Kyu-Ho Arifuzzaman, Sarder Pang, Won-Ki Ryu, Do-Yeal Song, Won-Hee Park, Yoo-Jin Pang, Myung-Geol Sci Rep Article In the past few years, bisphenol A, (BPA) an endocrine-disrupting chemical, has received increasing attention because of its detrimental health effects. There is ample evidence to support that BPA interferes with the reproductive health of humans and animals. In spermatozoa, BPA-induced adverse effects are mostly caused by increased oxidative stress. Using an in vitro experimental model, we examined whether antioxidants (glutathione, vitamin C, and vitamin E) have defensive effects against BPA-induced stress in spermatozoa. The results showed that antioxidants inhibit the overproduction of reactive oxygen species (basically cellular peroxides) and increase intracellular ATP levels, thereby preventing motility loss and abnormal acrosome reaction in BPA-exposed spermatozoa. In particular, glutathione and vitamin E reduced the protein kinase A-dependent tyrosine phosphorylation in spermatozoa and, thus, prevented the precocious acrosome reaction from occurring. Furthermore, we found that the compromised fertilisation and early embryo development mediated by BPA-exposed spermatozoa can be improved following their supplementation with glutathione and vitamin E. Based on these findings, we suggest that antioxidants reduce oxidative stress in BPA-exposed spermatozoa, thus preventing detrimental effects on their function and fertility. Nature Publishing Group UK 2019-07-22 /pmc/articles/PMC6646364/ /pubmed/31332285 http://dx.doi.org/10.1038/s41598-019-47158-9 Text en © The Author(s) 2019 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 Rahman, Md Saidur Kang, Kyu-Ho Arifuzzaman, Sarder Pang, Won-Ki Ryu, Do-Yeal Song, Won-Hee Park, Yoo-Jin Pang, Myung-Geol Effect of antioxidants on BPA-induced stress on sperm function in a mouse model |
title | Effect of antioxidants on BPA-induced stress on sperm function in a mouse model |
title_full | Effect of antioxidants on BPA-induced stress on sperm function in a mouse model |
title_fullStr | Effect of antioxidants on BPA-induced stress on sperm function in a mouse model |
title_full_unstemmed | Effect of antioxidants on BPA-induced stress on sperm function in a mouse model |
title_short | Effect of antioxidants on BPA-induced stress on sperm function in a mouse model |
title_sort | effect of antioxidants on bpa-induced stress on sperm function in a mouse model |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6646364/ https://www.ncbi.nlm.nih.gov/pubmed/31332285 http://dx.doi.org/10.1038/s41598-019-47158-9 |
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