Delay in oocyte aging in mice by the antioxidant N-acetyl-l-cysteine (NAC)

Liu, Jinmiao; Liu, Mengyuan; Ye, Xiaoying; Liu, Kai; Huang, Junjiu; Wang, Lingling; Ji, Guangzhen; Liu, Na; Tang, Xiang D.; Baltz, Jay M.; Keefe, David L.; Liu, Lin

doi:10.1093/humrep/des019

Cited by 140 publications

(108 citation statements)

References 70 publications

(77 reference statements)

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“…Our findings may gain importance as some researchers have recently shown that mice harboring gene mutations that promote chronic oxidative stress show accelerated ovarian aging [12]. Accordingly, other authors have demonstrated that the enrichment of the antioxidant defence against ROS is able to postpone the process of aging in mouse ovaries and oocytes [52, 53]. In addition, the treatment with N-acetylcysteine (NAC), a potent low-molecular weight intracellular antioxidant and precursor of GSH, has been shown to improve the follicular function and development by preventing oxidative stress [54].…”

Section: Discussionmentioning

confidence: 67%

Regular and Moderate Exercise Counteracts the Decline of Antioxidant Protection but Not Methylglyoxal-Dependent Glycative Burden in the Ovary of Reproductively Aging Mice

Falone

Santini

Cordone

et al. 2016

Oxidative Medicine and Cellular Longevity

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Population aging results in urgent needs of interventions aimed at ensuring healthy senescence. Exercise often results in healthy aging, yet many molecular mechanisms underlying such effects still need to be identified. We here investigated whether the age-dependent accumulation of oxidative and methylglyoxal- (MG-) related molecular damage could be delayed by moderate exercise in the mouse ovary, an organ that first exhibits impaired function with advancing age in mammals. CD1 female mice underwent two- or four-month treadmill-based running through the transition from adult to middle age, when ovaries show signs of senescence, and markers of protection against reactive oxygen species (ROS) and MG were measured. The long-term exercise reduced the protein oxidative damage in the ovaries (P < 0.01), and this was linked to the preservation of the glutathione peroxidase protection against ROS (P < 0.001), as well as to the increased glutathione availability (P < 0.001). Conversely, even though the age-related deactivation of the MG-targeting systems was partially prevented by the long-term running programme (P < 0.001), exercised mice were not protected from the age-dependent glycative burden. In summary, lately initiated regular and moderate exercise limited some changes occurring in the ovaries of middle-aged mice, and this might help to develop nonpharmacological cointerventions to reduce the vulnerability of mammalian ovaries towards redox dysfunctions.

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Section: Discussionmentioning

confidence: 67%

Regular and Moderate Exercise Counteracts the Decline of Antioxidant Protection but Not Methylglyoxal-Dependent Glycative Burden in the Ovary of Reproductively Aging Mice

Falone

Santini

Cordone

et al. 2016

Oxidative Medicine and Cellular Longevity

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“…Oral administration of antioxidants such as co-enzyme Q10, melatonin and N-acetyl-L-cysteine has been linked with improved oocyte quality, as well as increased fertilization rates and litter sizes in clinical and laboratory studies (Tamura et al 2008, Burstein et al 2009, Liu et al 2012; however, these reports focus primarily on the relationship between antioxidants and ovarian ageing. To the authors' knowledge, no in vivo studies have been conducted to establish the effects of orally administered antioxidants on post-ovulatory ageing specifically.…”

Section: Antioxidantsmentioning

confidence: 99%

Oxidative stress and ageing of the post-ovulatory oocyte

2013

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With extended periods of time following ovulation, the metaphase II stage oocyte experiences deterioration in quality referred to as post-ovulatory oocyte ageing. Post-ovulatory ageing occurs both in vivo and in vitro and has been associated with reduced fertilization rates, poor embryo quality, post-implantation errors and abnormalities in the offspring. Although the physiological consequences of post-ovulatory oocyte ageing have largely been established, the molecular mechanisms controlling this process are not well defined. This review analyses the relationships between biochemical changes exhibited by the ageing oocyte and the symptoms associated with the ageing phenotype. We also discuss molecular events that are potentially involved in orchestrating post-ovulatory ageing with a particular focus on the role of oxidative stress. We propose that oxidative stress may act as the initiator for a cascade of events that create the aged oocyte phenotype. Specifically, oxidative stress has the capacity to cause a decline in levels of critical cell cycle factors such as maturation-promoting factor, impair calcium homoeostasis, induce mitochondrial dysfunction and directly damage multiple intracellular components of the oocyte such as lipids, proteins and DNA. Finally, this review addresses current strategies for delaying post-ovulatory oocyte ageing with a particular focus on the potential use of compounds such as caffeine or selected antioxidants in the development of more refined media for the preservation of oocyte integrity during IVF procedures.

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“…There was an also slight improvement to oocyte spindle structure and a decrease in oocyte apoptosis in NAC-treated females. But, the number of oocytes retrieved at MII was not increased in aged females by NAC [ 67 ]. This highlights that age-induced oxidative damage to oocytes, not decreased ovarian reserve, is one cause of decreased fertility.…”

Section: Possible Therapiesmentioning

confidence: 84%