Mitochondrial Regulation of Spermatozoa Function: Metabolism, Oxidative Stress and Therapeutic Insights

Mitochondria are central to energy production and redox regulation in spermatozoa, supporting key functions such as progressive motility, capacitation, and the acrosome reaction. These processes are essential for successful fertilization and embryo development. However, species-specific differences...

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Main Authors: Zhiqian Xu, Qi Yan, Ke Zhang, Ying Lei, Chen Zhou, Tuanhui Ren, Ning Gao, Fengyun Wen, Xiaoxia Li
Format: Article
Language:English
Published: MDPI AG 2025-07-01
Series:Animals
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Online Access:https://www.mdpi.com/2076-2615/15/15/2246
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author Zhiqian Xu
Qi Yan
Ke Zhang
Ying Lei
Chen Zhou
Tuanhui Ren
Ning Gao
Fengyun Wen
Xiaoxia Li
author_facet Zhiqian Xu
Qi Yan
Ke Zhang
Ying Lei
Chen Zhou
Tuanhui Ren
Ning Gao
Fengyun Wen
Xiaoxia Li
author_sort Zhiqian Xu
collection DOAJ
description Mitochondria are central to energy production and redox regulation in spermatozoa, supporting key functions such as progressive motility, capacitation, and the acrosome reaction. These processes are essential for successful fertilization and embryo development. However, species-specific differences exist in the reliance on oxidative phosphorylation versus glycolysis. Mitochondria also generate reactive oxygen species, which at physiological levels aid in sperm function but can cause oxidative stress and damage when overproduced. Mitochondrial dysfunction and excessive ROS can impair membrane potential, induce apoptosis, and damage nuclear and mitochondrial DNA, ultimately compromising sperm quality. Sperm mitochondrial DNA is highly susceptible to mutations and deletions, contributing to reduced motility and fertility. Targeted antioxidant strategies have emerged as promising therapeutic interventions to mitigate oxidative damage. This article provides a comprehensive overview of mitochondrial regulation in spermatozoa, the consequences of redox imbalance, and the potential of mitochondria-targeted antioxidants to improve sperm function and male fertility outcomes. The paper aims to deepen our understanding of mitochondrial roles in sperm physiology and contribute to the advancement of strategies for addressing male infertility.
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publisher MDPI AG
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spelling doaj-art-140e19907eeb4ca1a14a2494df88d5f22025-08-20T04:00:49ZengMDPI AGAnimals2076-26152025-07-011515224610.3390/ani15152246Mitochondrial Regulation of Spermatozoa Function: Metabolism, Oxidative Stress and Therapeutic InsightsZhiqian Xu0Qi Yan1Ke Zhang2Ying Lei3Chen Zhou4Tuanhui Ren5Ning Gao6Fengyun Wen7Xiaoxia Li8College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, ChinaCollege of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, ChinaCollege of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, ChinaCollege of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, ChinaCollege of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, ChinaCollege of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, ChinaCollege of Animal Science and Technology, Hunan Agricultural University, Changsha 410125, ChinaCollege of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, ChinaCollege of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, ChinaMitochondria are central to energy production and redox regulation in spermatozoa, supporting key functions such as progressive motility, capacitation, and the acrosome reaction. These processes are essential for successful fertilization and embryo development. However, species-specific differences exist in the reliance on oxidative phosphorylation versus glycolysis. Mitochondria also generate reactive oxygen species, which at physiological levels aid in sperm function but can cause oxidative stress and damage when overproduced. Mitochondrial dysfunction and excessive ROS can impair membrane potential, induce apoptosis, and damage nuclear and mitochondrial DNA, ultimately compromising sperm quality. Sperm mitochondrial DNA is highly susceptible to mutations and deletions, contributing to reduced motility and fertility. Targeted antioxidant strategies have emerged as promising therapeutic interventions to mitigate oxidative damage. This article provides a comprehensive overview of mitochondrial regulation in spermatozoa, the consequences of redox imbalance, and the potential of mitochondria-targeted antioxidants to improve sperm function and male fertility outcomes. The paper aims to deepen our understanding of mitochondrial roles in sperm physiology and contribute to the advancement of strategies for addressing male infertility.https://www.mdpi.com/2076-2615/15/15/2246mitochondriaspermatozoaenergy metabolismreactive oxygen speciesmtDNAantioxidant
spellingShingle Zhiqian Xu
Qi Yan
Ke Zhang
Ying Lei
Chen Zhou
Tuanhui Ren
Ning Gao
Fengyun Wen
Xiaoxia Li
Mitochondrial Regulation of Spermatozoa Function: Metabolism, Oxidative Stress and Therapeutic Insights
Animals
mitochondria
spermatozoa
energy metabolism
reactive oxygen species
mtDNA
antioxidant
title Mitochondrial Regulation of Spermatozoa Function: Metabolism, Oxidative Stress and Therapeutic Insights
title_full Mitochondrial Regulation of Spermatozoa Function: Metabolism, Oxidative Stress and Therapeutic Insights
title_fullStr Mitochondrial Regulation of Spermatozoa Function: Metabolism, Oxidative Stress and Therapeutic Insights
title_full_unstemmed Mitochondrial Regulation of Spermatozoa Function: Metabolism, Oxidative Stress and Therapeutic Insights
title_short Mitochondrial Regulation of Spermatozoa Function: Metabolism, Oxidative Stress and Therapeutic Insights
title_sort mitochondrial regulation of spermatozoa function metabolism oxidative stress and therapeutic insights
topic mitochondria
spermatozoa
energy metabolism
reactive oxygen species
mtDNA
antioxidant
url https://www.mdpi.com/2076-2615/15/15/2246
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