Click here to close
Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly.
We suggest using a current version of Chrome,
FireFox, or Safari.
???displayArticle.abstract??? Egg overactivation occurs with a low frequency in the populations of naturally ovulated frog eggs. At present, its natural inducers, molecular mechanisms, and intracellular events remain unknown. Using microscopic and biochemical analyses, we demonstrate here that high levels of hydrogen peroxide-induced oxidative stress can cause time- and dose-dependent overactivation of Xenopus eggs. Lipofuscin accumulation, decrease of soluble cytoplasmic protein content, and depletion of intracellular ATP were found to take place in the overactivated eggs. Progressive development of these processes suggests that egg overactivation unfolds in a sequential and ordered fashion.
Figure 1. Morphological types of eggs observed in populations of naturally ovulated Xenopus eggs. Panels (a), (b), (c), and (d) present mature fertilization-competent, apoptotic, overactivated, and cortically contracted eggs, respectively. Panel (e) shows population of eggs matured in vitro in the presence of progesterone and aged by overnight incubation on bench. Arrows point to overactivated eggs.
Figure 2. Time and dose dependencies of egg overactivation by hydrogen peroxide. Panel (a) shows dynamics of morphological changes in the eggs overactivated by 100 mM hydrogen peroxide. Panel (b) presents time course of egg cortical contraction and overactivation after addition of 100 mM hydrogen peroxide. The untreated control (-H202) in panel (b) refers to overactivated phenotype. Panel (c) shows dose dependency of egg overactivation. Overactivated phenotype in panel (c) was counted in 240 min after addition of peroxide.
Figure 3. Oxidative stress-induced accumulation of lipofuscin in Xenopus eggs. Spot assay of lipofuscin autofluorescence in the insoluble particulate fractions of the peroxide-treated eggs and its quantification are presented in panels (a) and (b), respectively. The items labeled as 480∗ refer to control eggs incubated for 480 min in the absence of peroxide. Stars in panel (b) indicate statistical significance from the untreated control (p<0.05). Panel (c) shows SBB staining of the egg endosomal compartment. Hydrogen peroxide (f.c. 100 mM) was added to the eggs at 0 time.
Figure 4. Protein and ATP contents in overactivated Xenopus eggs. The contents of soluble cytosolic protein and intracellular ATP in the eggs overactivated by addition of 100 mM hydrogen peroxide are shown in panels (a) and (b), respectively. Control (Ctrl) in the panels refers to the eggs incubated for 480 min in the absence of hydrogen peroxide.
Bienert,
Membrane transport of hydrogen peroxide.
2006, Pubmed
Bienert,
Membrane transport of hydrogen peroxide.
2006,
Pubmed
Chebotareva,
Rat eggs cannot wait: Spontaneous exit from meiotic metaphase-II arrest.
2011,
Pubmed
Cui,
Oxidative stress, mitochondrial dysfunction, and aging.
2012,
Pubmed
Forman,
What is the concentration of hydrogen peroxide in blood and plasma?
2016,
Pubmed
Georgakopoulou,
Specific lipofuscin staining as a novel biomarker to detect replicative and stress-induced senescence. A method applicable in cryo-preserved and archival tissues.
2013,
Pubmed
Gómez-Sintes,
Lysosomal cell death mechanisms in aging.
2016,
Pubmed
Houel-Renault,
Autophagy is used as a survival program in unfertilized sea urchin eggs that are destined to die by apoptosis after inactivation of MAPK1/3 (ERK2/1).
2013,
Pubmed
Iguchi,
Unlaid Xenopus eggs degrade by apoptosis in the genital tract.
2013,
Pubmed
,
Xenbase
Kim,
Sodium selenite induces superoxide-mediated mitochondrial damage and subsequent autophagic cell death in malignant glioma cells.
2007,
Pubmed
Kirkland,
Loss of cardiolipin and mitochondria during programmed neuronal death: evidence of a role for lipid peroxidation and autophagy.
2002,
Pubmed
Lord,
Oxidative stress and ageing of the post-ovulatory oocyte.
2013,
Pubmed
Ma,
Reduced expression of MAD2, BCL2, and MAP kinase activity in pig oocytes after in vitro aging are associated with defects in sister chromatid segregation during meiosis II and embryo fragmentation after activation.
2005,
Pubmed
Masui,
Cytoplasmic control of nuclear behavior during meiotic maturation of frog oocytes.
1971,
Pubmed
Miao,
Oocyte aging: cellular and molecular changes, developmental potential and reversal possibility.
2009,
Pubmed
Moreira,
Increased autophagic degradation of mitochondria in Alzheimer disease.
2007,
Pubmed
Nikoletopoulou,
Crosstalk between apoptosis, necrosis and autophagy.
2013,
Pubmed
Philippe,
Different routes lead to apoptosis in unfertilized sea urchin eggs.
2014,
Pubmed
Prasad,
Morphological, cellular and molecular changes during postovulatory egg aging in mammals.
2015,
Pubmed
Premkumar,
An insufficient increase of cytosolic free calcium level results postovulatory aging-induced abortive spontaneous egg activation in rat.
2013,
Pubmed
Premkumar,
RyR channel-mediated increase of cytosolic free calcium level signals cyclin B1 degradation during abortive spontaneous egg activation in rat.
2014,
Pubmed
Sato,
Hydrogen peroxide induces Src family tyrosine kinase-dependent activation of Xenopus eggs.
2001,
Pubmed
,
Xenbase
Tokmakov,
Unfertilized frog eggs die by apoptosis following meiotic exit.
2011,
Pubmed
,
Xenbase
Tokmakov,
Postovulatory cell death: why eggs die via apoptosis in biological species with external fertilization.
2018,
Pubmed
Tokmakov,
Activity and intracellular localization of senescence-associated β-galactosidase in aging Xenopus oocytes and eggs.
2019,
Pubmed
,
Xenbase
Whitaker,
Calcium at fertilization and in early development.
2006,
Pubmed
,
Xenbase
Wu,
Raising Xenopus in the laboratory.
1991,
Pubmed
,
Xenbase
Xu,
Spontaneous activation of ovulated mouse eggs: time-dependent effects on M-phase exit, cortical granule exocytosis, maternal messenger ribonucleic acid recruitment, and inositol 1,4,5-trisphosphate sensitivity.
1997,
Pubmed
