Impact of Oxidative Stress on Age-Associated Decline in Oocyte Developmental Competence.
Hiroyuki Sasaki,Toshio Hamatani,Shintaro Kamijo,Maki Iwai,Masato Kobanawa,Seiji Ogawa,Kenji Miyado,Mamoru Tanaka +7 more
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TLDR
Increased ROS and increased vulnerability of oocytes to ROS lead to spindle instability, chromosomal abnormalities, telomere shortening, and reduced developmental competence of aged oocytes, focusing on oxidative stress (OS) in oocytes.Abstract:
Reproductive capacity in women starts to decline beyond their mid-30s and pregnancies in older women result in higher rates of miscarriage with aneuploidy. Age-related decline in fertility is strongly attributed to ovarian aging, diminished ovarian reserves, and decreased developmental competence of oocytes. In this review, we discuss the underlying mechanisms of age-related decline in oocyte quality, focusing on oxidative stress (OS) in oocytes. The primary cause is the accumulation of spontaneous damage to the mitochondria arising from increased reactive oxygen species (ROS) in oocytes, generated by the mitochondria themselves during daily biological metabolism. Mitochondrial dysfunction reduces ATP synthesis and influences the meiotic spindle assembly responsible for chromosomal segregation. Moreover, reproductively aged oocytes produce a decline in the fidelity of the protective mechanisms against ROS, namely the ROS-scavenging metabolism, repair of ROS-damaged DNA, and the proteasome and autophagy system for ROS-damaged proteins. Accordingly, increased ROS and increased vulnerability of oocytes to ROS lead to spindle instability, chromosomal abnormalities, telomere shortening, and reduced developmental competence of aged oocytes.read more
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Journal ArticleDOI
Mechanisms of oocyte aneuploidy associated with advanced maternal age.
TL;DR: The weight of evidence indicates that recombination failure, cohesin deterioration, spindle assembly checkpoint (SAC) disregulation, abnormalities in post-translational modification of histones and tubulin, and mitochondrial dysfunction are the leading causes of oocyte aneuploidy associated with maternal aging.
Journal ArticleDOI
Oxidative stress in oocyte aging and female reproduction.
TL;DR: In this paper, the relationship between reactive oxygen species (ROS) and antioxidants remain balanced and when the balance is broken toward an overabundance of ROS, oxidative stress appears and may lead to oocyte aging.
Journal ArticleDOI
The Role of Oxidative Stress and Natural Antioxidants in Ovarian Aging.
TL;DR: It is shown that oxidative stress plays a role in the etiology of ovarian aging and promotes the development of other ovarian aging-related etiologies, including telomere shortening, mitochondrial dysfunction, apoptosis, and inflammation, which raises the prospect of oxidative stress modulator-natural antioxidants as therapeutic interventions for delaying ovarian aging.
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Melatonin regulates the activities of ovary and delays the fertility decline in female animals via MT1/AMPK pathway.
Lu Zhang,Zhenzhen Zhang,Jing Wang,Dongying Lv,Tianqi Zhu,Feng Wang,Xiuzhi Tian,Yao Yujun,Pengyun Ji,Guoshi Liu +9 more
TL;DR: It is convincingly proven that melatonin administration delays ovary aging and improves fertility in mice via MT1/AMPK pathway.
Journal ArticleDOI
Mitochondrial Dysfunction and Oxidative Stress Caused by Cryopreservation in Reproductive Cells.
Roberto Gualtieri,Guruprasad Kalthur,Vincenza Barbato,Maddalena Di Nardo,Satish Kumar Adiga,Riccardo Talevi +5 more
TL;DR: In this paper, the role played by mitochondria and ROS in sperm and oocyte function and the close, biunivocal relationships between mitochondrial damage and ROS generation during cryopreservation of gametes and gonadal tissues in different species.
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