scholarly journals Glycine ameliorates mitochondrial dysfunction caused by ABT-199 in porcine oocytes

2021 ◽  
Author(s):  
Sicong Yu ◽  
Lepeng Gao ◽  
Yang Song ◽  
Xin Ma ◽  
Shuang Liang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Oocyte Maturation ◽  
Mitochondrial Function ◽  
Protective Action ◽  
Damage Model ◽  
Developmental Competence ◽  
Free Calcium ◽  
Maturation In Vitro

Abstract Mitochondria play an important role in controlling oocyte developmental competence. Our previous studies showed that glycine can regulate mitochondrial function and improve oocyte maturation in vitro. However, the mechanisms by which glycine affects mitochondrial function during oocyte maturation in vitro have not been fully investigated. In this study, we induced a mitochondrial damage model in oocytes with the Bcl-2-specific antagonist ABT-199. We investigated whether glycine could reverse the mitochondrial dysfunction induced by ABT-199 exposure and whether it is related to calcium regulation. Our results showed that ABT-199 inhibited cumulus expansion, decreased the oocyte maturation rate and the intracellular glutathione (GSH) level, caused mitochondrial dysfunction, induced oxidative stress, which was confirmed by decreased mitochondrial membrane potential (Δ⍦m) and the expression of mitochondrial function-related genes (PGC-1α), and increased reactive oxygen species (ROS) levels and the expression of apoptosis-associated genes (Bax, caspase-3, CytC). More importantly, ABT-199-treated oocytes showed an increase in the intracellular free calcium concentration ([Ca 2+]i) and had impaired cortical type 1 inositol 1,4,5-trisphosphate receptors (IP3R1) distribution. Nevertheless, treatment with glycine significantly ameliorated mitochondrial dysfunction, oxidative stress and apoptosis, glycine also regulated [Ca 2+]i levels and IP3R1 cellular distribution, which further protects oocyte maturation in ABT-199-induced porcine oocytes. Taken together, our results indicate that glycine has a protective action against ABT-199-induced mitochondrial dysfunction in porcine oocytes.

scholarly journals Perfluorononanoic acid impedes mouse oocyte maturation by inducing mitochondrial dysfunction and oxidative stress

2021 ◽  
Author(s):  
Xiaofei Jiao ◽  
Ning Liu ◽  
Yiding Xu ◽  
Huanyu Qiao
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Oocyte Maturation ◽  
Early Stage ◽  
Spindle Assembly ◽  
Mouse Oocyte ◽  
Toxic Effects ◽  
Germinal Vesicle Breakdown ◽  
Maturation In Vitro

Perfluorononanoic acid (PFNA), a member of PFAS, is frequently detected in human blood and tissues, even in follicular fluid of women. The exposure of PFNA, but not PFOA and PFOS, is positively correlated with miscarriage and increased time to pregnancy. Toxicological studies indicated that PFNA exposure is associated with immunotoxicity, hepatotoxicity, developmental toxicity, and reproductive toxicity in animals. However, there is little information regarding the toxic effects of PFNA on oocyte maturation. In this study, we investigated the toxic effects of PFNA exposure on mouse oocyte maturation in vitro. Our results showed that 600 μM PFNA significantly inhibited germinal vesicle breakdown (GVBD) and polar body extrusion (PBE) in mouse oocytes. Our further study revealed that PFNA induced abnormal metaphase I (MI) spindle assembly, evidenced by malformed spindles and mislocalization of p-ERK1/2 in PFNA-treated oocytes. We also found that PFNA induced abnormal mitochondrial distribution and increased mitochondrial membrane potential. Consequently, PFNA increased reactive oxygen species (ROS) levels, leading to oxidative stress, DNA damage, and eventually early-stage apoptosis in oocytes. In addition, after 14 h culture, PFNA disrupted the formation of metaphase II (MII) spindle in most PFNA-treated oocytes with polar bodies. Collectively, our results indicate that PFNA interferes with oocyte maturation in vitro via disrupting spindle assembly, damaging mitochondrial functions, and inducing oxidative stress, DNA damage, and early-stage apoptosis.

scholarly journals Maturation of human oocytes in vitro and their developmental competence

Reproduction ◽  
2001 ◽  
pp. 51-75 ◽  
Author(s):  
A Trounson ◽  
C Anderiesz ◽  
G Jones
Keyword(s):  
Embryo Development ◽  
Oocyte Maturation ◽  
Growth Phase ◽  
Developmental Competence ◽  
Minimum Size ◽  
Success Rates ◽  
Human Oocytes ◽  
Maturation In Vitro

Complete maturation of oocytes is essential for the developmental competence of embryos. Any interventions in the growth phase of the oocyte and the follicle in the ovary will affect oocyte maturation, fertilization and subsequent embryo development. Oocyte size is associated with maturation and embryo development in most species examined and this may indicate that a certain size is necessary to initiate the molecular cascade of normal nuclear and cytoplasmic maturation. The minimum size of follicle required for developmental competence in humans is 5-7 mm in diameter. Maturation in vitro can be accomplished in humans, but is associated with a loss of developmental competence unless the oocyte is near completion of its preovulatory growth phase. This loss of developmental competence is associated with the absence of specific proteins in oocytes cultured to metaphase II in vitro. The composition of culture medium used successfully for maturation of human oocytes is surprisingly similar to that originally developed for maturation of oocytes in follicle culture in vitro. The presence of follicle support cells in culture is necessary for the gonadotrophin-mediated response required to mature oocytes in vitro. Gonadotrophin concentration and the sequence of FSH and FSH-LH exposure may be important for human oocytes, particularly those not exposed to the gonadotrophin surge in vivo. More research is needed to describe the molecular and cellular events, the presence of checkpoints and the role of gene expression, translation and protein uptake on completing oocyte maturation in vitro and in vivo. In the meantime, there are very clear applications for maturing oocytes in human reproductive medicine and the success rates achieved in some of these special applications are clinically valuable.

scholarly journals Effect of Triclosan Exposure on Developmental Competence in Parthenogenetic Porcine Embryo during Preimplantation

2020 ◽  
Vol 21 (16) ◽  
pp. 5790
Author(s):  
Min Ju Kim ◽  
Hyo-Jin Park ◽  
Sanghoon Lee ◽  
Hyo-Gu Kang ◽  
Pil-Soo Jeong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Embryonic Development ◽  
Mitochondrial Dysfunction ◽  
Formation Rate ◽  
Developmental Competence ◽  
Early Embryonic Development ◽  
Toxic Effects ◽  
Blastocyst Formation ◽  
Parthenogenetic Embryos

Triclosan (TCS) is included in various healthcare products because of its antimicrobial activity; therefore, many humans are exposed to TCS daily. While detrimental effects of TCS exposure have been reported in various species and cell types, the effects of TCS exposure on early embryonic development are largely unknown. The aim of this study was to determine if TCS exerts toxic effects during early embryonic development using porcine parthenogenetic embryos in vitro. Porcine parthenogenetic embryos were cultured in in vitro culture medium with 50 or 100 µM TCS for 6 days. Developmental parameters including cleavage and blastocyst formation rates, developmental kinetics, and the number of blastomeres were assessed. To determine the toxic effects of TCS, apoptosis, oxidative stress, and mitochondrial dysfunction were assessed. TCS exposure resulted in a significant decrease in 2-cell rate and blastocyst formation rate, as well as number of blastomeres, but not in the cleavage rate. TCS also increased the number of apoptotic blastomeres and the production of reactive oxygen species. Finally, TCS treatment resulted in a diffuse distribution of mitochondria and decreased the mitochondrial membrane potential. Our results showed that TCS exposure impaired porcine early embryonic development by inducing DNA damage, oxidative stress, and mitochondrial dysfunction.

Impact of gonadotropins on oocyte maturation, fertilisation and developmental competence in vitro

2014 ◽  
Vol 26 (5) ◽  
pp. 752 ◽  
Author(s):  
Xuemei Wang ◽  
Tony Tsai ◽  
Jie Qiao ◽  
Zhan Zhang ◽  
Huai L. Feng
Keyword(s):  
Oocyte Maturation ◽  
Early Embryo ◽  
Developmental Competence ◽  
Dependent Manner ◽  
Success Rates ◽  
Maturation In Vitro ◽  
High Concentrations ◽  
Development In Vitro ◽  
Dose Dependent

The aim of the present study was to evaluate the dose-dependent effects of gonadotropins, either singly (Bravelle (B), Luveris (L), Menupur (M), Repronex (R), Gonal-F (G), Follism (F) and Norvarel (N)) or in combination (Menupur + Bravelle; Repronext + Bravelle; and Bravelle + Norvarel), on rates of oocyte maturation, fertilisation and early embryo development in vitro in an animal model. Bovine cumulus–oocyte complexes (COCs) were purchased commercially and cultured in TCM-199 with 10% fetal bovine serum supplemented with varying concentrations of gonadotropin (0, 5, 10, 20, 40 IU or United States Pharmacopoeia (USP) mL–1) for 24 and 48 h according to current IVF clinical stimulation protocols. All gonadotropins enhanced oocyte maturation in vitro in a dose-dependent manner. Individually, Gonal-F (Merck KGaA, Darmstadt, Germany), Follism (Merck Co, Whitehouse Station, NJ, USA) and Repronext (Ferring, Parsippany, NJ, USA) promoted oocyte maturation; in combination, they effectively enhanced COC expansion and increased the maturation competence of MII oocytes. However, high concentrations of gonadotropins may result in maturation arrest. Specific combinations of gonadotropins may change the rate of early embryonic development (8–16-cells) and morula–blastocyst formation. These data provide support for the responsiveness of bovine oocytes to gonadotropins in vitro and the need to consider variations in the relative concentrations and ratio of combinations (FSH/LH or human chorionic gonadotropin) for optimisation of oocyte developmental competence. The results of the present study could be applied to therapeutic clinical stimulation protocols and help improve IVF success rates.

scholarly journals Iron Overload-Induced Ferroptosis Impairs Porcine Oocyte Maturation and Subsequent Embryonic Developmental Competence in vitro

2021 ◽  
Vol 9 ◽  
Author(s):  
Weiyi Hu ◽  
Yan Zhang ◽  
Dali Wang ◽  
Tingting Yang ◽  
Jiajia Qi ◽  
...  
Keyword(s):  
Cell Death ◽  
Iron Overload ◽  
Mitochondrial Dysfunction ◽  
Oocyte Maturation ◽  
Oocyte Quality ◽  
Developmental Competence ◽  
Ammonium Citrate ◽  
Regulated Cell Death ◽  
Porcine Oocyte

Accumulating evidence indicates that ferroptosis is an iron-dependent form of regulated cell death. This type of iron-dependent programmed cell death is different from traditional forms of regulated cell death, such as apoptosis and autophagy. However, the role of ferroptosis in porcine oocyte maturation and the associated mechanism remain unclear. In the present research, we investigated the effects of ferric ammonium citrate (FAC), a specific ferroptosis inducer, on porcine oocyte meiotic maturation and quality and subsequent embryonic developmental competence. FAC treatment caused obvious accumulation of intracellular ferrous ions in porcine oocytes. At the end of the in vitro maturation (IVM) period, there was a significant decrease in the polar body (PB) extrusion rate and an increase in the percentage of abnormal oocytes in the FAC treatment groups, indicating that iron overload-induced ferroptosis may suppress the meiotic process during porcine oocyte maturation. We also found that after FAC treatment, the subsequent two-cell rate, four-cell rate and blastocyst formation rate were significantly decreased in porcine parthenogenetic activation (PA) embryos, indicating that iron overload-induced ferroptosis decreased porcine oocyte quality. Further analysis revealed that FAC treatment not only enhanced intracellular reactive oxygen species (ROS) generation, decreased intracellular free thiol levels and induced mitochondrial dysfunction but also triggered autophagy in porcine oocytes. Taken together, these findings suggest that iron overload-induced ferroptosis impairs porcine oocyte meiosis and decreases porcine oocyte quality, possibly by increasing oxidative stress, inducing mitochondrial dysfunction and triggering autophagy.

scholarly journals Rosmarinic acid treatment during porcine oocyte maturation attenuates oxidative stress and improves subsequent embryo development in vitro

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e6930
Author(s):  
Yan Zhang ◽  
Jing Guo ◽  
Xiao Wei Nie ◽  
Zi Yue Li ◽  
Yu Meng Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oocyte Maturation ◽  
Rosmarinic Acid ◽  
Reactive Oxygen Species Generation ◽  
Subsequent Development ◽  
Developmental Competence ◽  
Control Group ◽  
Porcine Oocyte ◽  
Number Of Cells

Background In vitro maturation (IVM) of oocytes has been widely used in the field of assisted reproductive technology. However, oocytes can be injured by oxidative stress during the process of IVM. Methods The present study was designed to evaluate the influences of rosmarinic acid (RA) on the IVM of porcine oocytes and the subsequent development of early-stage embryos as well as its underlying mechanisms. Various concentrations of RA (5 µM, 10 µM, and 25 µM) were treated with porcine oocyte maturation medium during the period of IVM. Results and Discussion The results showed that 5 µM RA treatment during the period of porcine oocyte IVM improves blastocyst quality and hatching ability after parthenogenetic activation. Furthermore, the presence of RA during the period of IVM dramatically improved the total number of cells after somatic cell nuclear transfer compared to the number of cells in the control group. Notably, RA treatment during the period of porcine oocyte IVM decreased intracellular reactive oxygen species generation not only in oocytes but also in cumulus cells. Further analysis showed that the intracellular free thiols levels in the oocytes were enhanced by treatment with RA during the period of porcine oocyte IVM compared to the free thiols levels in the control groups. These results indicate that RA improves the developmental competence of porcine oocytes during the IVM period by attenuating oxidative stress.

scholarly journals Phytochemicals from Cocoa Shell Protect Mitochondrial Function and Alleviate Oxidative Stress in Hepatocytes via Regulation of ERK and PI3K-AKT Pathways

2021 ◽  
Vol 2 (1) ◽  
pp. 25
Author(s):  
Miguel Rebollo-Hernanz ◽  
Yolanda Aguilera ◽  
Maria A. Martin-Cabrejas ◽  
Elvira Gonzalez de Mejia
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Aqueous Extract ◽  
Mitochondrial Function ◽  
Nonalcoholic Fatty Liver ◽  
Atp Production ◽  
Mitochondrial Superoxide ◽  
Cocoa Shell ◽  
The Impact

This research aimed to assess the impact of an aqueous extract from the cocoa shell and its major phytochemicals on preventing oxidative stress and mitochondrial dysfunction in hepatocytes using an in vitro model of nonalcoholic fatty liver disease (NAFLD). The phytochemicals from cocoa shell were extracted using water and characterized by UPLC-MS/MS analysis. HepG2 cells were cotreated with either the aqueous extract from cocoa shell (CAE, 20–100 µg mL−1) or 10–50 µmol L−1 of pure theobromine, protocatechuic acid, procyanidin B2, epicatechin, and catechin in the presence or absence of palmitic acid (PA, 500 µmol L−1) to mimic NAFLD conditions in vitro. Biomarkers of mitochondrial function and oxidative stress were evaluated 24 h after the cotreatment in cell supernatants and lysates using chemical, biochemical, and immunochemical techniques. CAE and the phytochemicals therein significantly (p < 0.05) protected mitochondrial content (15–100%) and preserved mitochondrial function, promoting O2 consumption (1.2- to 1.8-fold) and ATP production (1.3- to 2.1-fold). Phytochemicals from cocoa shell significantly (p < 0.05) decreased PA-triggered oxidative stress. The mitochondrial membrane potential was maintained (62–100%), and the production of mitochondrial superoxide (26–100%) and total ROS (17–100%) was abrogated. CAE significantly (p < 0.05) modulated cell signaling pathways associated with ROS production and mitochondrial dysfunction, including an increase in the phosphorylation of ERK1/2 (2.8-fold), protein kinase B (AKT) (2.8-fold), GSK3 (2.3-fold), Raf-1 (1.9-fold), and mTOR (1.7-fold). In conclusion, results suggested that the cocoa shell’s phytochemicals could protect mitochondrial liver function and alleviate oxidative stress by modulating key pathways involved in their regulation.

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