Bisphenol A induces testicular oxidative stress in mice leading to ferroptosis

Bisphenol A is a common environmental factor and endocrine disruptor that exerts a negative impact on male reproductive ability. By exploring bisphenol A-induced testicular cell death using the Institute of Cancer Research (ICR) mouse model, we found that a ferroptosis phenomenon may exist. Mice wer...

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Main Authors: Li Li, Min-Yan Wang, Hua-Bo Jiang, Chun-Rong Guo, Xian-Dan Zhu, Xia-Qin Yao, Wei-Wei Zeng, Yuan Zhao, Ling-Kan Chi
Format: Article
Language:English
Published: Wolters Kluwer Medknow Publications 2023-01-01
Series:Asian Journal of Andrology
Subjects:
Online Access:http://www.ajandrology.com/article.asp?issn=1008-682X;year=2023;volume=25;issue=3;spage=375;epage=381;aulast=
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author Li Li
Min-Yan Wang
Hua-Bo Jiang
Chun-Rong Guo
Xian-Dan Zhu
Xia-Qin Yao
Wei-Wei Zeng
Yuan Zhao
Ling-Kan Chi
author_facet Li Li
Min-Yan Wang
Hua-Bo Jiang
Chun-Rong Guo
Xian-Dan Zhu
Xia-Qin Yao
Wei-Wei Zeng
Yuan Zhao
Ling-Kan Chi
author_sort Li Li
collection DOAJ
description Bisphenol A is a common environmental factor and endocrine disruptor that exerts a negative impact on male reproductive ability. By exploring bisphenol A-induced testicular cell death using the Institute of Cancer Research (ICR) mouse model, we found that a ferroptosis phenomenon may exist. Mice were divided into six groups and administered different doses of bisphenol A via intragastric gavage once daily for 45 consecutive days. Serum was then collected to determine the levels of superoxide dismutase and malondialdehyde. Epididymal sperm was also collected for semen analysis, and testicular tissue was collected for ferritin content determination, electron microscope observation of mitochondrial morphology, immunohistochemistry, real-time quantitative polymerase chain reaction, and western blot analysis. Exposure to bisphenol A was found to decrease sperm quality and cause oxidative damage, iron accumulation, and mitochondrial damage in the testes of mice. In addition, bisphenol A was confirmed to affect the expression of the ferroptosis-related genes, glutathione peroxidase 4 (GPX4), ferritin heavy chain 1 (FTH1), cyclooxygenase 2 (COX2), and acyl-CoA synthetase 4 (ACSL4) in mouse testicular tissues. Accordingly, we speculate that bisphenol A induces oxidative stress, which leads to the ferroptosis of testicular cells. Overall, the inhibition of ferroptosis may be a potential strategy to reduce male reproductive toxicity caused by bisphenol A.
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spelling doaj.art-ba18f4d77eb0454081fd2b158a11766b2023-05-18T04:59:34ZengWolters Kluwer Medknow PublicationsAsian Journal of Andrology1008-682X1745-72622023-01-0125337538110.4103/aja202266Bisphenol A induces testicular oxidative stress in mice leading to ferroptosisLi LiMin-Yan WangHua-Bo JiangChun-Rong GuoXian-Dan ZhuXia-Qin YaoWei-Wei ZengYuan ZhaoLing-Kan ChiBisphenol A is a common environmental factor and endocrine disruptor that exerts a negative impact on male reproductive ability. By exploring bisphenol A-induced testicular cell death using the Institute of Cancer Research (ICR) mouse model, we found that a ferroptosis phenomenon may exist. Mice were divided into six groups and administered different doses of bisphenol A via intragastric gavage once daily for 45 consecutive days. Serum was then collected to determine the levels of superoxide dismutase and malondialdehyde. Epididymal sperm was also collected for semen analysis, and testicular tissue was collected for ferritin content determination, electron microscope observation of mitochondrial morphology, immunohistochemistry, real-time quantitative polymerase chain reaction, and western blot analysis. Exposure to bisphenol A was found to decrease sperm quality and cause oxidative damage, iron accumulation, and mitochondrial damage in the testes of mice. In addition, bisphenol A was confirmed to affect the expression of the ferroptosis-related genes, glutathione peroxidase 4 (GPX4), ferritin heavy chain 1 (FTH1), cyclooxygenase 2 (COX2), and acyl-CoA synthetase 4 (ACSL4) in mouse testicular tissues. Accordingly, we speculate that bisphenol A induces oxidative stress, which leads to the ferroptosis of testicular cells. Overall, the inhibition of ferroptosis may be a potential strategy to reduce male reproductive toxicity caused by bisphenol A.http://www.ajandrology.com/article.asp?issn=1008-682X;year=2023;volume=25;issue=3;spage=375;epage=381;aulast=bisphenol a; ferroptosis; mitochondrial damage; oxidative stress; testicular toxicity
spellingShingle Li Li
Min-Yan Wang
Hua-Bo Jiang
Chun-Rong Guo
Xian-Dan Zhu
Xia-Qin Yao
Wei-Wei Zeng
Yuan Zhao
Ling-Kan Chi
Bisphenol A induces testicular oxidative stress in mice leading to ferroptosis
Asian Journal of Andrology
bisphenol a; ferroptosis; mitochondrial damage; oxidative stress; testicular toxicity
title Bisphenol A induces testicular oxidative stress in mice leading to ferroptosis
title_full Bisphenol A induces testicular oxidative stress in mice leading to ferroptosis
title_fullStr Bisphenol A induces testicular oxidative stress in mice leading to ferroptosis
title_full_unstemmed Bisphenol A induces testicular oxidative stress in mice leading to ferroptosis
title_short Bisphenol A induces testicular oxidative stress in mice leading to ferroptosis
title_sort bisphenol a induces testicular oxidative stress in mice leading to ferroptosis
topic bisphenol a; ferroptosis; mitochondrial damage; oxidative stress; testicular toxicity
url http://www.ajandrology.com/article.asp?issn=1008-682X;year=2023;volume=25;issue=3;spage=375;epage=381;aulast=
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