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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 4015874, 22 pages
Review Article

Molecular Mechanisms Responsible for Increased Vulnerability of the Ageing Oocyte to Oxidative Damage

1Priority Research Centre for Reproductive Science, School of Environmental and Life Sciences, University of Newcastle, Callaghan, NSW, Australia
2School of Biological Sciences, University of Auckland, Auckland, New Zealand

Correspondence should be addressed to Bettina P. Mihalas; ua.ude.nou@salahim.anitteb and Brett Nixon; ua.ude.eltsacwen@noxin.tterb

Received 24 May 2017; Accepted 3 August 2017; Published 18 October 2017

Academic Editor: Tanea T. Reed

Copyright © 2017 Bettina P. Mihalas et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


In their midthirties, women experience a decline in fertility, coupled to a pronounced increase in the risk of aneuploidy, miscarriage, and birth defects. Although the aetiology of such pathologies are complex, a causative relationship between the age-related decline in oocyte quality and oxidative stress (OS) is now well established. What remains less certain are the molecular mechanisms governing the increased vulnerability of the aged oocyte to oxidative damage. In this review, we explore the reduced capacity of the ageing oocyte to mitigate macromolecular damage arising from oxidative insults and highlight the dramatic consequences for oocyte quality and female fertility. Indeed, while oocytes are typically endowed with a comprehensive suite of molecular mechanisms to moderate oxidative damage and thus ensure the fidelity of the germline, there is increasing recognition that the efficacy of such protective mechanisms undergoes an age-related decline. For instance, impaired reactive oxygen species metabolism, decreased DNA repair, reduced sensitivity of the spindle assembly checkpoint, and decreased capacity for protein repair and degradation collectively render the aged oocyte acutely vulnerable to OS and limits their capacity to recover from exposure to such insults. We also highlight the inadequacies of our current armoury of assisted reproductive technologies to combat age-related female infertility, emphasising the need for further research into mechanisms underpinning the functional deterioration of the ageing oocyte.