Protection against reactive oxygen species during mouse preimplantation embryo development: Role of EDTA, oxygen tension, catalase, superoxide dismutase and pyruvate

2001 ◽  
Vol 59 (1) ◽  
pp. 44-53 ◽  
Author(s):  
Nicolas M. Orsi ◽  
Henry J. Leese
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Oxygen Tension ◽  
Embryo Development ◽  
Preimplantation Embryo ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Preimplantation Embryo Development ◽  
Mouse Preimplantation Embryo

Ionomycin-induced mouse oocyte activation can disrupt preimplantation embryo development through increased reactive oxygen species reaction and DNA damage

2020 ◽  
Vol 26 (10) ◽  
pp. 773-783
Author(s):  
Chen Chen ◽  
Tingye Sun ◽  
Mingru Yin ◽  
Zhiguang Yan ◽  
Weina Yu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Energy Metabolism ◽  
Embryo Development ◽  
Preimplantation Embryo ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Oocyte Activation ◽  
Preimplantation Embryo Development ◽  
Normal Fertilization

Abstract Oocyte activation induced by calcium oscillations is an important process in normal fertilization and subsequent embryogenesis. In the clinical-assisted reproduction, artificial oocyte activation (AOA) is an effective method to improve the clinical outcome of patients with null or low fertilization rate after ICSI. However, little is known about the effect of AOA on preimplantation embryo development in cases with normal fertilization by ICSI. Here, we used ionomycin at different concentrations to activate oocytes after ICSI with normal sperm and evaluated energy metabolism and preimplantation embryo development. We found that a high concentration of ionomycin increased the frequency and amplitude of calcium oscillation patterns, affecting the balance of mitochondrial energy metabolism, leading to increased reactive oxygen species (ROS) and decreased ATP. Eventually, it increases DNA damage and decreases blastocyst formation. In addition, the addition of vitamin C to the culture medium ameliorated the increase in ROS and DNA damage and rescued the abnormal embryo development caused by excessive ionomycin activation. This study provides a perspective that the improper application of AOA may have adverse effects on preimplantation embryo development. Thus, clinical AOA treatment should be cautiously administered.

277 EFFECTS OF ERYTHROCYTE AND ERYTHROCYTE HEMOLYSATE ON BOVINE PREIMPLANTATION EMBRYO DEVELOPMENT IN VITRO UNDER REACTIVE OXYGEN SPECIES CONDITION

2010 ◽  
Vol 22 (1) ◽  
pp. 295
Author(s):  
A. Ideta ◽  
K. Tsuchiya ◽  
Y. Nakamura ◽  
M. Urakawa ◽  
M. Murakami ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Embryo Development ◽  
Reactive Oxygen ◽  
Hemoglobin Concentration ◽  
Blastocyst Stage ◽  
Preimplantation Embryos ◽  
Oxygen Species ◽  
Preimplantation Embryo Development ◽  
Presence And Absence

Reactive oxygen species (ROS) damage preimplantation embryos by increasing DNA fragmentation, leading to early embryonic death. Erythrocytes have been shown to protect other cells and tissues against ROS. In mice, erythrocytes were recently found to improve the early development of embryos by their antioxidant effect. The purpose of the present study was to examine the effect of erythrocytes on the in vitro development of bovine IVF embryos in medium supplemented with ROS. COCs were aspirated from ovaries collected from a local slaughterhouse and were cultured for 22 h in TCM-199 containing 5% fetal bovine serum. IVF was performed using an IVF100 (Research Institute for the Functional Peptides, Yamagata, Japan) according to the manufacturer’s instructions. In experiment 1, IVF embryos were cultured in CR1aa medium supplemented with an oxidizing agent, 0.5 mM hypoxanthine and 0.01 U mL-1 xanthine oxidase (HX/XOD), in the presence and absence of erythrocytes (5 × 104, 5× 105, 5×106, and 5 × 107 erythrocytes mL-1). In experiments 2 and 3, the development of embryos under the condition without ROS was assessed in the presence and absence of erythrocytes (5 × 106 erythrocytes mL-1) or erythrocyte hemolysate (hemoglobin concentration of 1.9 g L-1), respectively. At 7 days after in vitro culture, the development to the blastocyst stage of IVF embryos was examined using a stereomicroscope. Data were analyzed using Fisher’s PLSD test and Student’s t-test In experiment 1, the presence of HX/XOD significantly inhibited embryo development to the blastocyst stage in vitro (P < 0.05). The addition of erythrocytes to medium supplemented with HX/XOD markedly improved preimplantation development (Table 1). In experiments 2 and 3, supplementation of erythrocytes or erythrocyte hemolysate promoted the development of embryos to the blastocyst stage (experiment 2: erythrocyte 42.4 ± 3.1%, control 28.5 ± 5.7%, P < 0.1; experiment 3: erythrocyte hemolysate 39.1 ± 3.3%, control 30.2 ± 1.0%, P < 0.1). In conclusion, we suggest that the addition of erythrocytes to culture medium can counteract the negative effects of ROS on embryo development and blastocyst formation. Table 1.Effect of HX/XOD and erythrocyte supplementation on embryo development to blastocyst stage

scholarly journals Reactive oxygen species mediate arachidonic acid-induced dilation in porcine coronary microvessels

2003 ◽  
Vol 285 (6) ◽  
pp. H2309-H2315 ◽  
Author(s):  
Christine L. Oltman ◽  
Neal L. Kane ◽  
Francis J. Miller ◽  
Arthur A. Spector ◽  
Neal L. Weintraub ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Arachidonic Acid ◽  
Coronary Arteries ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cox Inhibitors ◽  
Ros Scavenger ◽  
Krebs Buffer

Reactive oxygen species (ROS) have been proposed to mediate vasodilation in the microcirculation. We investigated the role of ROS in arachidonic acid (AA)-induced coronary microvascular dilation. Porcine epicardial coronary arterioles (110 ± 4 μm diameter) were mounted onto pipettes in oxygenated Krebs buffer. Vessels were incubated with vehicle or 1 mM Tiron (a nonselective ROS scavenger), 250 U/ml polyethylene-glycolated (PEG)-superoxide dismutase (SOD; an [Formula: see text] scavenger), 250 U/ml PEG-catalase (a H2O2 scavenger), or the cyclooxygenase (COX) inhibitors indomethacin (10 μM) or diclofenac (10 μM) for 30 min. After endothelin constriction (30–60% of resting diameter), cumulative concentrations of AA (10–10–10–5 M) were added and internal diameters measured by video microscopy. AA (10–7 M) produced 37 ± 6% dilation, which was eliminated by the administration of indomethacin (4 ± 7%, P < 0.05) or diclofenac (–8 ± 8%, P < 0.05), as well as by Tiron (–4 ± 5%, P < 0.05), PEG-SOD (–10 ± 6%, P < 0.05), or PEG-catalase (1 ± 4%, P < 0.05). Incubation of small coronary arteries with [3H]AA resulted in the formation of prostaglandins, which was blocked by indomethacin. In separate studies in microvessels, AA induced concentration-dependent increases in fluorescence of the oxidant-sensitive probe dichlorodihydrofluorescein diacetate, which was inhibited by pretreatment with indomethacin or by SOD + catalase. We conclude that in porcine coronary microvessels, COX-derived ROS contribute to AA-induced vasodilation.

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