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Review
. 2019 Nov 22:10:811.
doi: 10.3389/fendo.2019.00811. eCollection 2019.

Impact of Oxidative Stress on Age-Associated Decline in Oocyte Developmental Competence

Hiroyuki Sasaki  1 , Toshio Hamatani  1 , Shintaro Kamijo  1 , Maki Iwai  1 , Masato Kobanawa  1 , Seiji Ogawa  1 , Kenji Miyado  2 , Mamoru Tanaka  1
Affiliations
Review

Impact of Oxidative Stress on Age-Associated Decline in Oocyte Developmental Competence

Hiroyuki Sasaki et al. Front Endocrinol (Lausanne). .

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.

Keywords: ER stress; antioxidants; mitochondrial dysfunction; oocyte aging; oxidative stree.

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Figures

Figure 1
Figure 1
Possible mechanism of aged oocyte deterioration with accumulating oxidative stress. External ROS, AGEs, and accumulation of internal ROS from mitochondria are burdening oocytes as oxidative stress (OS). Then, OS induces deterioration of mitochondria, telomere shortening, spindle formation error, DNA damage, and protein degradation. ROS, reactive oxygen species. AGEs, glycation end-products. RAGE, receptor for advanced glycation end-products. 4-HNE, 4-hydroxynonenal.
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