scholarly journals Effects of Fungicide Euparen Multi (Tolylfluanid) on Development of Preimplantation Embryos in Mouse

2007 ◽  
Vol 76 (2) ◽  
pp. 209-214 ◽  
Author(s):  
M. Domaracký ◽  
P. Rehák ◽  
J. Legáth ◽  
J. Koppel
Keyword(s):  
Cell Death ◽  
Preimplantation Embryo ◽  
Preimplantation Embryos ◽  
Hoechst 33342 ◽  
Preimplantation Embryo Development ◽  
Cell Numbers ◽  
Calcein Am ◽  
Dose Dependent ◽  
Triple Staining ◽  
Different Doses

The effect of the fungicide Euparen Multi (containing 50% tolylfluanid) on the development of mouse preimplantation embryos was evaluated. Euparen Multi was daily administered per os to female mice (ICR strain) at four different doses of 118, 294, 588 and 1177 mg/kg b.m., beginning on day 1 of pregnancy. Embryos obtained on day 4 of pregnancy were stained by morphological triple staining (Hoechst 33342, propidium iodide, Calcein AM), and the number of nuclei, blastocyst formation, distribution of embryos according to the nucleus number and cell death incidence were determined. Embryos in the experimental groups (except for the lowest dose 118 mg/kg b.m.) showed a highly significant dose-dependent reduction in total cell numbers corresponding to the lower proportion of blastocysts. The occurrence of cell death was significantly increased in all experimental groups, indicating that Euparen Multi is able to cause cell death at relatively low doses. Our data demonstrate that Euparen Multi could induce significant alterations in the preimplantation embryo development.

scholarly journals Inhibition of DRP1 Impedes Zygotic Genome Activation and Preimplantation Development in Mice

2021 ◽  
Vol 9 ◽  
Author(s):  
Yuanyuan Li ◽  
Ning-Hua Mei ◽  
Gui-Ping Cheng ◽  
Jing Yang ◽  
Li-Quan Zhou
Keyword(s):  
Embryo Development ◽  
Preimplantation Embryo ◽  
Preimplantation Embryos ◽  
Dependent Manner ◽  
Zygotic Genome Activation ◽  
Preimplantation Embryo Development ◽  
Cell Embryo ◽  
Embryo Stage ◽  
Genome Activation ◽  
Zygotic Genome

Mitochondrion plays an indispensable role during preimplantation embryo development. Dynamic-related protein 1 (DRP1) is critical for mitochondrial fission and controls oocyte maturation. However, its role in preimplantation embryo development is still lacking. In this study, we demonstrate that inhibition of DRP1 activity by mitochondrial division inhibitor-1, a small molecule reported to specifically inhibit DRP1 activity, can cause severe developmental arrest of preimplantation embryos in a dose-dependent manner in mice. Meanwhile, DRP1 inhibition resulted in mitochondrial dysfunction including decreased mitochondrial activity, loss of mitochondrial membrane potential, reduced mitochondrial copy number and inadequate ATP by disrupting both expression and activity of DRP1 and mitochondrial complex assembly, leading to excessive ROS production, severe DNA damage and cell cycle arrest at 2-cell embryo stage. Furthermore, reduced transcriptional and translational activity and altered histone modifications in DRP1-inhibited embryos contributed to impeded zygotic genome activation, which prevented early embryos from efficient development beyond 2-cell embryo stage. These results show that DRP1 inhibition has potential cytotoxic effects on mammalian reproduction, and DRP1 inhibitor should be used with caution when it is applied to treat diseases. Additionally, this study improves our understanding of the crosstalk between mitochondrial metabolism and zygotic genome activation.

Effects of progesterone antagonists RU486 and ZK98734 on embryo transport, development and implantation in laboratory mice

1990 ◽  
Vol 2 (6) ◽  
pp. 713 ◽  
Author(s):  
A Vinijsanun ◽  
L Martin
Keyword(s):  
Preimplantation Embryo ◽  
Normal Embryo ◽  
Laboratory Mice ◽  
Mouse Uterus ◽  
Preimplantation Embryo Development ◽  
Epithelial Morphology ◽  
Progestin Treatment ◽  
Embryo Transport ◽  
Dose Dependent

Two progesterone antagonists blocked the actions of progesterone on uterine mitosis and epithelial morphology, but had no oestrogenic, anti-oestrogenic, cytotoxic or gestagenic activities in the mouse uterus. They interrupted early pregnancy and were luteolytic. These actions were reversed by treatment with exogenous progestins, but not dexamethasone. Doses of antagonists which blocked pregnancy and were luteolytic induced premature entry of embryos into the uterus on Day 3 and loss from the tract by Day 4. With the more potent RU486, most embryos remaining in the tract on Day 4 were in the oviduct. This 'tube-locking' and accelerated loss were probably due to 'unopposed' actions of ovarian oestrogen. They were reversed by progestin treatment; this suggests that progesterone is essential for normal embryo transport. Doses of antagonists which prevented normal embryo transport and implantation had little effect on preimplantation embryo development. Small increases in numbers of abnormal embryos on Day 4 were not significant or dose dependent. Abnormalities were not correlated with location of embryos, nor prevented by progestin treatment which reversed antagonist effects on embryo transport and implantation. Hence, progesterone is apparently not essential for successful completion of preimplantation development of mouse embryos in vivo.

scholarly journals Phosphatidylinositol 3-kinase signaling in mammalian preimplantation embryo development

Reproduction ◽  
2008 ◽  
Vol 136 (2) ◽  
pp. 147-156 ◽  
Author(s):  
Chris O'Neill
Keyword(s):  
Embryo Development ◽  
Normal Development ◽  
Preimplantation Embryo ◽  
Preimplantation Embryos ◽  
External Information ◽  
Ph Domain ◽  
Phosphatidylinositol 3 Kinase ◽  
Preimplantation Embryo Development ◽  
Wide Range ◽  
Phosphatidylinositol 3

The development of the preimplantation mammalian embryo is an autopoietic process; once initiated development proceeds without an absolute requirement for external information or growth cues. This developmental autonomy is partly explained by the generation of autocrine trophic ligands that are released and act back on the embryo via specific receptors. Several embryotrophic ligands cause receptor-dependent activation of 1-o-phosphatidylinositol 3-kinase. This enzyme phosphorylates phosphatidylinositol-4,5-bisphosphate to form phosphatidylinositol-3,4,5-trisphosphate. Genetic or pharmacological ablation of this enzyme activity disrupts normal development of preimplantation embryos. Phosphatidylinositol-3,4,5-trisphosphate is a membrane lipid that acts as a docking site for a wide range of proteins possessing the pleckstrin homology (PH) domain. Such proteins are important regulators of cell survival, proliferation, and differentiation. RAC-α serine/threonine protein kinase is an important PH domain protein and its activity is required for normal preimplantation embryo development and survival. The activity of a range of PH domain proteins is also implicated in the normal development of the embryo. This review critically examines the evidence for the activation of 1-o-phosphatidylinositol 3-kinase in the generation of pleiotypic trophic response to embryotrophins in the autopoietic development of the preimplantation embryo.

scholarly journals Deadly decisions: the role of genes regulating programmed cell death in human preimplantation embryo development

Reproduction ◽  
2004 ◽  
Vol 128 (3) ◽  
pp. 281-291 ◽  
Author(s):  
Andrea Jurisicova ◽  
Beth M Acton
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Cell Fate ◽  
Embryo Development ◽  
Preimplantation Embryo ◽  
Culture Media ◽  
Culture Conditions ◽  
Early Embryo ◽  
Preimplantation Embryo Development

Human preimplantation embryo development is prone to high rates of early embryo wastage, particularly under currentin vitroculture conditions. There are many possible underlying causes for embryo demise, including DNA damage, poor embryo metabolism and the effect of suboptimal culture media, all of which could result in an imbalance in gene expression and the failed execution of basic embryonic decisions. In view of the complex interactions involved in embryo development, a thorough understanding of these parameters is essential to improving embryo quality. An increasing body of evidence indicates that cell fate (i.e. survival/differentiation or death) is determined by the outcome of specific intracellular interactions between pro- and anti-apoptotic proteins, many of which are expressed during oocyte and preimplantation embryo development. The recent availability of mutant mice lacking expression of various genes involved in the regulation of cell survival has enabled rapid progress towards identifying those molecules that are functionally important for normal oocyte and preimplantation embryo development. In this review we will discuss the current understanding of the regulation of cell death gene expression during preimplantation embryo development, with a focus on human embryology and a discussion of animal models where appropriate.

scholarly journals Intracellular oxygen metabolism during bovine oocyte and preimplantation embryo development

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Paul J. McKeegan ◽  
Selina F. Boardman ◽  
Amy A. Wanless ◽  
Grace Boyd ◽  
Laura J. Warwick ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Oxygen Consumption ◽  
Oxygen Concentration ◽  
Embryo Development ◽  
Preimplantation Embryo ◽  
Complex Iii ◽  
Preimplantation Embryos ◽  
Mitochondrial Oxygen Consumption ◽  
Preimplantation Embryo Development

AbstractWe report a novel method to profile intrcellular oxygen concentration (icO2) during in vitro mammalian oocyte and preimplantation embryo development using a commercially available multimodal phosphorescent nanosensor (MM2). Abattoir-derived bovine oocytes and embryos were incubated with MM2 in vitro. A series of inhibitors were applied during live-cell multiphoton imaging to record changes in icO2 associated with mitochondrial processes. The uncoupler carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP) uncouples mitochondrial oxygen consumption to its maximum, while antimycin inhibits complex III to ablate mitochondrial oxygen consumption. Increasing oxygen consumption was expected to reduce icO2 and decreasing oxygen consumption to increase icO2. Use of these inhibitors quantifies how much oxygen is consumed at basal in comparison to the upper and lower limits of mitochondrial function. icO2 measurements were compared to mitochondrial DNA copy number analysed by qPCR. Antimycin treatment increased icO2 for all stages tested, suggesting significant mitochondrial oxygen consumption at basal. icO2 of oocytes and preimplantation embryos were unaffected by FCCP treatment. Inner cell mass icO2 was lower than trophectoderm, perhaps reflecting limitations of diffusion. Mitochondrial DNA copy numbers were similar between stages in the range 0.9–4 × 106 copies and did not correlate with icO2. These results validate the MM2 probe as a sensitive, non-toxic probe of intracellular oxygen concentration in mammalian oocytes and preimplantation embryos.

scholarly journals From cell death to embryo arrest: Mathematical models of human preimplantation embryo development

2001 ◽  
Vol 98 (4) ◽  
pp. 1655-1660 ◽  
Author(s):  
K. Hardy ◽  
S. Spanos ◽  
D. Becker ◽  
P. Iannelli ◽  
R. M. L. Winston ◽  
...  
Keyword(s):  
Cell Death ◽  
Mathematical Models ◽  
Embryo Development ◽  
Preimplantation Embryo ◽  
Preimplantation Embryo Development

Exposure to mono-n-butyl phthalate disrupts the development of preimplantation embryos

2013 ◽  
Vol 25 (8) ◽  
pp. 1174 ◽  
Author(s):  
Da-Peng Chu ◽  
Shi Tian ◽  
Da-Guang Sun ◽  
Chan-Juan Hao ◽  
Hong-Fei Xia ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Methylation ◽  
Dibutyl Phthalate ◽  
Preimplantation Embryo ◽  
Blastocyst Stage ◽  
Preimplantation Embryos ◽  
Oxygen Species ◽  
Preimplantation Embryo Development ◽  
Immunofluorescent Analysis ◽  
Butyl Phthalate

Dibutyl phthalate (DBP), a widely used phthalate, is known to cause many serious diseases, especially in the reproductive system. However, little is known about the effects of its metabolite, mono-n-butyl phthalate (MBP), on preimplantation embryo development. In the present study, we found that treatment of embryos with 10–3 M MBP impaired developmental competency, whereas exposure to 10–4 M MBP delayed the progression of preimplantation embryos to the blastocyst stage. Furthermore, reactive oxygen species (ROS) levels in embryos were significantly increased following treatment with 10–3 M MBP. In addition, 10–3 M MBP increased apoptosis via the release of cytochrome c, whereas immunofluorescent analysis revealed that exposure of preimplantation embryos to MBP concentration-dependently (10–5, 10–4 and 10–3 M) decreased DNA methylation. Together, the results indicate a possible relationship between MBP exposure and developmental failure in preimplantation embryos.

Osteopontin is expressed in the oviduct and promotes fertilization and preimplantation embryo development of mouse

Zygote ◽  
2014 ◽  
Vol 23 (4) ◽  
pp. 622-630 ◽  
Author(s):  
Qian Liu ◽  
Qing-zhen Xie ◽  
Yun Zhou ◽  
Jing Yang
Keyword(s):  
Estrous Cycle ◽  
Embryo Development ◽  
Preimplantation Embryo ◽  
Normal Pregnancy ◽  
Vital Role ◽  
Antibody Treatment ◽  
Preimplantation Embryo Development ◽  
Mrna And Protein Expression ◽  
Dose Dependent

SummaryOsteopontin (OPN) is a multifunctional phosphoprotein that is detected in various tissues, including male and female reproductive tracts. In this study, we evaluated OPN expression in mouse oviducts during the estrus cycle, and at days 1–5 of pregnancy and pseudopregnancy by reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. The mice oocytes, sperm and embryos were treated with different concentrations of anti-OPN antibody in vitro to detect the function of OPN in fertilization and preimplantation embryo development. OPN mRNA and protein expression in mouse oviducts were cyclic dependent throughout the estrous cycle, which was highest at estrous and lowest at diestrous. Such a phenomenon was consistent with the change in estrogen level in mice. The expression levels of OPN in mice oviduct of normal pregnancy and pseudopregnancy were significantly different, which indicated that OPN expression in mouse oviducts was depend on estrogen and preimplantation embryo. Furthermore, anti-OPN antibody treatment could reduce the rates of fertilization, cleavage and blastocyst formation in vitro in a dose-dependent way. Overall, our results indicated that the expression of OPN in mouse oviducts during the estrous cycle and early pregnancy is likely regulated by estrogen and the embryo, and OPN may play a vital role in oocyte fertilization and preimplantation embryo development.

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