Age-Related Decline of Male Fertility: Mitochondrial Dysfunction and the Antioxidant Interventions

Mitochondria are structurally and functionally unique organelles in male gametes. Apparently, as the only organelles remaining in mature sperm, mitochondria not only produce adeno-sine triphosphate (ATP) through oxidative phosphorylation (OXPHOS) to support sperm mobility, but also play key roles in...

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Main Authors: Jing-Jing Wang, Shu-Xia Wang, Tehmina, Yan Feng, Rui-Fen Zhang, Xin-Yue Li, Qiong Sun, Jian Ding
Format: Article
Language:English
Published: MDPI AG 2022-04-01
Series:Pharmaceuticals
Subjects:
Online Access:https://www.mdpi.com/1424-8247/15/5/519
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author Jing-Jing Wang
Shu-Xia Wang
Tehmina
Yan Feng
Rui-Fen Zhang
Xin-Yue Li
Qiong Sun
Jian Ding
author_facet Jing-Jing Wang
Shu-Xia Wang
Tehmina
Yan Feng
Rui-Fen Zhang
Xin-Yue Li
Qiong Sun
Jian Ding
author_sort Jing-Jing Wang
collection DOAJ
description Mitochondria are structurally and functionally unique organelles in male gametes. Apparently, as the only organelles remaining in mature sperm, mitochondria not only produce adeno-sine triphosphate (ATP) through oxidative phosphorylation (OXPHOS) to support sperm mobility, but also play key roles in regulating reactive oxidation species (ROS) signaling, calcium homeostasis, steroid hormone biosynthesis, and apoptosis. Mitochondrial dysfunction is often associated with the aging process. Age-dependent alterations of the epididymis can cause alterations in sperm mitochondrial functioning. The resultant cellular defects in sperm have been implicated in male infertility. Among these, oxidative stress (OS) due to the overproduction of ROS in mitochondria may represent one of the major causes of these disorders. Excessive ROS can trigger DNA damage, disturb calcium homeostasis, impair OXPHOS, disrupt the integrity of the sperm lipid membrane, and induce apoptosis. Given these facts, scavenging ROS by antioxidants hold great potential in terms of finding promising therapeutic strategies to treat male infertility. Here, we summarize the progress made in understanding mitochondrial dysfunction, aging, and male infertility. The clinical potential of antioxidant interventions was also discussed.
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spelling doaj.art-44df54c5aecd453da012471ab0e668f42023-11-23T12:33:50ZengMDPI AGPharmaceuticals1424-82472022-04-0115551910.3390/ph15050519Age-Related Decline of Male Fertility: Mitochondrial Dysfunction and the Antioxidant InterventionsJing-Jing Wang0Shu-Xia Wang1Tehmina2Yan Feng3Rui-Fen Zhang4Xin-Yue Li5Qiong Sun6Jian Ding7School of Life Science and Technology, Xi’an Jiaotong University, Xi’an 710049, ChinaSchool of Life Science and Technology, Xi’an Jiaotong University, Xi’an 710049, ChinaSchool of Life Science and Technology, Xi’an Jiaotong University, Xi’an 710049, ChinaSchool of Life Science and Technology, Xi’an Jiaotong University, Xi’an 710049, ChinaSchool of Life Science and Technology, Xi’an Jiaotong University, Xi’an 710049, ChinaSchool of Life Science and Technology, Xi’an Jiaotong University, Xi’an 710049, ChinaSchool of Life Science and Technology, Xi’an Jiaotong University, Xi’an 710049, ChinaSchool of Life Science and Technology, Xi’an Jiaotong University, Xi’an 710049, ChinaMitochondria are structurally and functionally unique organelles in male gametes. Apparently, as the only organelles remaining in mature sperm, mitochondria not only produce adeno-sine triphosphate (ATP) through oxidative phosphorylation (OXPHOS) to support sperm mobility, but also play key roles in regulating reactive oxidation species (ROS) signaling, calcium homeostasis, steroid hormone biosynthesis, and apoptosis. Mitochondrial dysfunction is often associated with the aging process. Age-dependent alterations of the epididymis can cause alterations in sperm mitochondrial functioning. The resultant cellular defects in sperm have been implicated in male infertility. Among these, oxidative stress (OS) due to the overproduction of ROS in mitochondria may represent one of the major causes of these disorders. Excessive ROS can trigger DNA damage, disturb calcium homeostasis, impair OXPHOS, disrupt the integrity of the sperm lipid membrane, and induce apoptosis. Given these facts, scavenging ROS by antioxidants hold great potential in terms of finding promising therapeutic strategies to treat male infertility. Here, we summarize the progress made in understanding mitochondrial dysfunction, aging, and male infertility. The clinical potential of antioxidant interventions was also discussed.https://www.mdpi.com/1424-8247/15/5/519mitochondriareactive oxidation speciesagingantioxidantmale infertility
spellingShingle Jing-Jing Wang
Shu-Xia Wang
Tehmina
Yan Feng
Rui-Fen Zhang
Xin-Yue Li
Qiong Sun
Jian Ding
Age-Related Decline of Male Fertility: Mitochondrial Dysfunction and the Antioxidant Interventions
Pharmaceuticals
mitochondria
reactive oxidation species
aging
antioxidant
male infertility
title Age-Related Decline of Male Fertility: Mitochondrial Dysfunction and the Antioxidant Interventions
title_full Age-Related Decline of Male Fertility: Mitochondrial Dysfunction and the Antioxidant Interventions
title_fullStr Age-Related Decline of Male Fertility: Mitochondrial Dysfunction and the Antioxidant Interventions
title_full_unstemmed Age-Related Decline of Male Fertility: Mitochondrial Dysfunction and the Antioxidant Interventions
title_short Age-Related Decline of Male Fertility: Mitochondrial Dysfunction and the Antioxidant Interventions
title_sort age related decline of male fertility mitochondrial dysfunction and the antioxidant interventions
topic mitochondria
reactive oxidation species
aging
antioxidant
male infertility
url https://www.mdpi.com/1424-8247/15/5/519
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