Contrast in Levels of Metabolic Enzymes in Human and Mouse Ova1

M.‐Y., Maggie; Manchester, Jill K.; Yang, Victoria C.; Curato, Andrea D.; Strickler, Ronald C.; Lowry, Oliver H.

doi:10.1095/biolreprod39.2.295

Cited by 80 publications

(63 citation statements)

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“…The role of Ca 2C rise in egg activation and cortical granule release is well established in mouse (Tombes et al 1992). A decreased intracytoplasmic level of ATP (Chi et al 1988) and increased intracellular Ca 2C and reduction of the endoplasmic reticulum Ca 2C have been observed in aged oocytes, and the increase in intracellular Ca 2C has been attributed to dysfunction of the endoplasmic reticulum Ca 2C -ATPase in these oocytes (Vincent et al 1992, Igarashi et al 1997, Takahashi et al 2000. Moreover, our recent experiments showed that rotenone, a mitochondrial inhibitor, accelerated mouse oocyte aging in the presence of pyruvate (data to be published).…”

Section: Pyruvate and Oocyte Agingmentioning

confidence: 99%

Pyruvate prevents aging of mouse oocytes

Liu

Wu²,

Lan³

et al. 2009

Reproduction

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Inhibiting oocyte aging is important not only for healthy reproduction but also for the success of assisted reproduction techniques. Although our previous studies showed that cumulus cells accelerated aging of mouse oocytes, the underlying mechanism is unknown. The objective of this paper was to study the effects of pyruvate and cumulus cells on mouse oocyte aging. Freshly ovulated mouse cumulus-oocyte complexes (COCs) or cumulus-denuded oocytes (DOs) were cultured in Chatot-Ziomek-Bavister (CZB) medium or COC-conditioned CZB medium supplemented with different concentrations of pyruvate before being examined for aging signs and developmental potential. Pyruvate supplementation to CZB medium decreased rates of ethanol-induced activation in both COCs and DOs by maintaining their maturation-promoting factor activities, but more pyruvate was needed for COCs than for DOs. Addition of pyruvate to the COC-conditioned CZB also alleviated aging of DOs. Observations on cortical granules, level of BCL2 proteins, histone acetylation, intracellular concentration of glutathione, and embryo development all confirmed that pyruvate supplementation inhibited aging of mouse oocytes. It is concluded that the aging of mouse oocytes, facilitated by culture in COCs, can be partially prevented by the addition of pyruvate to the culture medium.

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Section: Pyruvate and Oocyte Agingmentioning

confidence: 99%

Pyruvate prevents aging of mouse oocytes

Liu

Wu²,

Lan³

et al. 2009

Reproduction

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“…The functionality of the mitochondria does, however, become compromised with extended periods of time following ovulation, a factor that is thought to heavily influence oocyte quality. Diminished mitochondrial integrity in the in vitro aged oocyte has been demonstrated by a loss of mitochondrial membrane potential (Zhang et al 2011) and a decline in levels of ATP production (Chi et al 1988).…”

Section: Mitochondrial Dysfunctionmentioning

confidence: 99%

“…Oxidative stress has been linked with mtDNA damage and deletions (Sohal & Dubey 1994), loss of mitochondrial membrane potential (Liu et al 2000), increased ROS generation by the ETC (Liu et al 2009a) and a decline in ATP production (Melov et al 1999). Importantly, factors such as increased ROS generation and a decline of ATP production are also known to be associated with postovulatory ageing (Chi et al 1988, Lord et al 2013, suggesting that a link between oxidative stress and agerelated mitochondrial dysfunction is certainly plausible. Notably, oxidative damage to mtDNA in the oocyte could potentially be the basis for the aforementioned abnormalities associated with impaired mitochondrial function in offspring originating from aged oocytes (Tarin et al 2002).…”

Section: Mitochondrial Dysfunctionmentioning

confidence: 99%

“…Post-ovulatory aged oocytes exhibit numerous aberrations in their cell biology including partial cortical granule exocytosis (Szollosi 1971, Dodson et al 1989, Ducibella et al 1990, Xu et al 1997, zona hardening (Longo 1981, Dodson et al 1989, Xu et al 1997, a decrease in critical cell cycle factors including maturation-promoting factor (MPF) and MAPK (Kikuchi et al 2002), mitochondrial dysfunction (Chi et al 1988, Takahashi et al 2003, Tatone et al 2011, Zhang et al 2011, Lord et al 2013, spindle abnormalities (Wakayama et al 2004), losses of chromosomal integrity (Spielmann et al 1985, Mailhes et al 1998, Wakayama et al 2004) and epigenetic changes (Liang et al 2008; Table 1). Not surprisingly, the process of post-ovulatory ageing culminates in apoptosis (Fujino et al 1996) as a result of decreases in expression of the anti-apoptotic protein BCL2 (Gordo et al 2002, Ma et al 2005) and the activation of caspases (Takai et al 2007, Lord et al 2013.…”

Section: Introductionmentioning

confidence: 99%

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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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“…The assay was performed in a 50 mM Tris buffer at pH 7.7 containing 40 mM aspartate, 2 mM ␣-ketoglutarate, 80 M NADH, and 40 units of malate dehydrogenase (14). For each enzyme assay the enzyme extraction was thawed and expelled under oil onto a siliconised glass slide and kept at 4°C until analysis was completed (around 10 min).…”

Section: Media-mentioning

confidence: 99%

Mitochondrial Malate-Aspartate Shuttle Regulates Mouse Embryo Nutrient Consumption

Lane

Gardner

2005

Journal of Biological Chemistry

106

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Pyruvate has been considered the sole substrate that can support development of the mouse zygote to the two-cell stage, with lactate able to support development from the two-cell stage. This study has determined for the first time that mitochondrial reducing equivalent shuttles regulate metabolism in the early embryo. Activity of the malate-aspartate shuttle was found to be essential for the metabolism of lactate in the two-cell embryo. Furthermore, the inability of the mouse zygote to use lactate as an energy source was a result of a lack of malate-aspartate shuttle activity. The mRNA for the four enzymes for shuttle activity were detected at all stages of development. It was determined that aspartate was a rate-limiting factor in the activity of the malate-aspartate shuttle in mouse zygotes probably due to the high K m of the cytoplasmic aspartate aminotransferase. Addition of high concentrations of exogenous aspartate to the culture medium enabled mouse zygotes to utilize lactate in the absence of pyruvate and develop normally to the blastocyst stage as well as produce normal viable offspring. This study determined that the malateaspartate shuttle is a key regulator of embryo metabolism and therefore viability and is the first report that mouse zygotes can develop normally to term in the absence of pyruvate.Studies on the preimplantation mouse embryo have indicated that the zygote has an absolute requirement for pyruvate to complete the first cleavage division (1-3). Significantly, lactate is only able to support development from the two-cell stage (4), and glucose could support development from the eight-cell stage (5). Interestingly, mouse zygotes can metabolize both pyruvate and lactate (6, 7) even though cleavage only occurs in the presence of pyruvate. While this has been documented for more than 30 years, there is no explanation for this unusual pattern of metabolism at the zygote nor is it known what changes occur in the embryo that enable the two-cell embryo to use lactate to support development.Energy metabolism in cells is compartmentalized to either the cytoplasm or the mitochondria. Pyruvate is transported into the mitochondria by specific transport proteins and is metabolized within the mitochondria. In contrast, lactate is converted to pyruvate within the cytosol with the concomitant conversion of NAD ϩ to NADH. Cells must maintain a balance of metabolic intermediates between the cytosol and the mitochondria to enable lactate metabolism to continue. An inability to maintain this balance results in impairment of either mitochondrial and/or cytoplasmic metabolism. In addition to many enzymes existing in either the cytoplasm or mitochondria, the pyridine nucleotides (NAD ϩ , NADH, NADP ϩ , and NADPH) are also compartmentalized between the cytoplasm and the mitochondria. Intact mitochondria are impermeable to NADH (8). Therefore to transfer NADH across the mitochondrial membrane for oxidation and ATP production and for the regeneration of cytoplasmic NAD ϩ , there is an indirect pathway involving th...

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Contrast in Levels of Metabolic Enzymes in Human and Mouse Ova1

Cited by 80 publications

References 0 publications

Pyruvate prevents aging of mouse oocytes

Pyruvate prevents aging of mouse oocytes

Oxidative stress and ageing of the post-ovulatory oocyte

Mitochondrial Malate-Aspartate Shuttle Regulates Mouse Embryo Nutrient Consumption

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