4.7 Review

Mitochondrial Functionality in Male Fertility: From Spermatogenesis to Fertilization

Journal

ANTIOXIDANTS
Volume 10, Issue 1, Pages -

Publisher

MDPI
DOI: 10.3390/antiox10010098

Keywords

mitochondria; oxidative phosphorylation; spermatozoa; male infertility; testis; epididymis; capacitation; fertilization

Funding

  1. Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education [NRF-2020R1C1C1003380]

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Mitochondria play crucial roles in male fertility by providing energy, regulating sperm development and acidity, and participating in testosterone production. Male infertility is mainly associated with the loss of mitochondrial proteins, leading to reduced sperm motility and infertility.
Mitochondria are structurally and functionally distinct organelles that produce adenosine triphosphate (ATP) through oxidative phosphorylation (OXPHOS), to provide energy to spermatozoa. They can also produce reactive oxidation species (ROS). While a moderate concentration of ROS is critical for tyrosine phosphorylation in cholesterol efflux, sperm-egg interaction, and fertilization, excessive ROS generation is associated with male infertility. Moreover, mitochondria participate in diverse processes ranging from spermatogenesis to fertilization to regulate male fertility. This review aimed to summarize the roles of mitochondria in male fertility depending on the sperm developmental stage (from male reproductive tract to female reproductive tract). Moreover, mitochondria are also involved in testosterone production, regulation of proton secretion into the lumen to maintain an acidic condition in the epididymis, and sperm DNA condensation during epididymal maturation. We also established the new signaling pathway using previous proteomic data associated with male fertility, to understand the overall role of mitochondria in male fertility. The pathway revealed that male infertility is associated with a loss of mitochondrial proteins in spermatozoa, which induces low sperm motility, reduces OXPHOS activity, and results in male infertility.

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