Mechanism of the Reduction of an Oxidized Glutathione Peroxidase Mimic with Thiols

2012 ◽  
Vol 8 (12) ◽  
pp. 5052-5057 ◽  
Author(s):  
Gavin S. Heverly-Coulson ◽  
Russell J. Boyd
Keyword(s):  
Glutathione Peroxidase ◽  
Oxidized Glutathione ◽  
Peroxidase Mimic

scholarly journals Xenopus gpx3 Mediates Posterior Development by Regulating Cell Death during Embryogenesis

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1265
Author(s):  
Hongchan Lee ◽  
Tayaba Ismail ◽  
Youni Kim ◽  
Shinhyeok Chae ◽  
Hong-Yeoul Ryu ◽  
...  
Keyword(s):  
Cell Death ◽  
Embryonic Development ◽  
Glutathione Peroxidase ◽  
Critical Role ◽  
Model Organism ◽  
Bmp Signaling ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Peroxidase Mimic ◽  
Tail Region ◽  
Stage Of Development

Glutathione peroxidase 3 (GPx3) belongs to the glutathione peroxidase family of selenoproteins and is a key antioxidant enzyme in multicellular organisms against oxidative damage. Downregulation of GPx3 affects tumor progression and metastasis and is associated with liver and heart disease. However, the physiological significance of GPx3 in vertebrate embryonic development remains poorly understood. The current study aimed to investigate the functional roles of gpx3 during embryogenesis. To this end, we determined gpx3’s spatiotemporal expression using Xenopus laevis as a model organism. Using reverse transcription polymerase chain reaction (RT-PCR), we demonstrated the zygotic nature of this gene. Interestingly, the expression of gpx3 enhanced during the tailbud stage of development, and whole mount in situ hybridization (WISH) analysis revealed gpx3 localization in prospective tail region of developing embryo. gpx3 knockdown using antisense morpholino oligonucleotides (MOs) resulted in short post-anal tails, and these malformed tails were significantly rescued by glutathione peroxidase mimic ebselen. The gene expression analysis indicated that gpx3 knockdown significantly altered the expression of genes associated with Wnt, Notch, and bone morphogenetic protein (BMP) signaling pathways involved in tailbud development. Moreover, RNA sequencing identified that gpx3 plays a role in regulation of cell death in the developing embryo. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and phospho-histone 3 (PH3) staining confirmed the association of gpx3 knockdown with increased cell death and decreased cell proliferation in tail region of developing embryos, establishing the involvement of gpx3 in tailbud development by regulating the cell death. Furthermore, these findings are inter-related with increased reactive oxygen species (ROS) levels in gpx3 knockdown embryos, as measured by using a redox-sensitive fluorescent probe HyPer. Taken together, our results suggest that gpx3 plays a critical role in posterior embryonic development by regulating cell death and proliferation during vertebrate embryogenesis.

scholarly journals Synthesis of alpha‐methyl selenocysteine and its utilization as a glutathione peroxidase mimic

2019 ◽  
Vol 25 (6) ◽  
pp. e3173 ◽  
Author(s):  
Robert J. Wehrle ◽  
Emma J. Ste.Marie ◽  
Robert J. Hondal ◽  
Douglas S. Masterson
Keyword(s):  
Glutathione Peroxidase ◽  
Peroxidase Mimic

scholarly journals Engineering Glutathione Transferase to a Novel Glutathione Peroxidase Mimic With High Catalytic Efficiency

2005 ◽  
Vol 280 (12) ◽  
pp. 11930-11935 ◽  
Author(s):  
Hui-jun Yu ◽  
Jun-qiu Liu ◽  
August Böck ◽  
Jing Li ◽  
Gui-min Luo ◽  
...  
Keyword(s):  
Glutathione Peroxidase ◽  
Glutathione Transferase ◽  
Catalytic Efficiency ◽  
Peroxidase Mimic

Modeling the Mechanism of the Glutathione Peroxidase Mimic Ebselen

2011 ◽  
Vol 50 (23) ◽  
pp. 12075-12084 ◽  
Author(s):  
Sonia Antony ◽  
Craig A. Bayse
Keyword(s):  
Glutathione Peroxidase ◽  
Peroxidase Mimic

scholarly journals Characterization of Oxidative Stress in Various Tissues of Diabetic and Galactose-fed Rats

2001 ◽  
Vol 2 (3) ◽  
pp. 211-216 ◽  
Author(s):  
Robert M. Strother ◽  
Tonya G. Thomas ◽  
Mary Otsyula ◽  
Ruth A. Sanders ◽  
John B. Watkins III
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Rat Model ◽  
Catalase Activity ◽  
Diabetic Rats ◽  
Oxidized Glutathione ◽  
Hepatic Glutathione ◽  
Reduced And Oxidized Glutathione

Rats fed a galactose-rich diet have been used for several years as a model for diabetes to study, particularly in the eye, the effects of excess blood hexoses. This study sought to determine the utility of galactosemia as a model for oxidative stress in extraocular tissues by examining biomarkers of oxidative stress in galactose-fed rats and experimentally-induced diabetic rats. Sprague-Dawley rats were divided into four groups: experimental control; streptozotocin-induced diabetic; insulin-treated diabetic; and galactose-fed. The rats were maintained on these regimens for 30 days, at which point the activities of catalase, glutathione peroxidase, glutathione reductase, and superoxide dismutase, as well as levels of lipid peroxidation and reduced and oxidized glutathione were determined in heart, liver, and kidney. This study indicates that while there are some similarities between galactosemic and diabetic rats in these measured indices of oxidative stress (hepatic catalase activity levels and hepatic and renal levels of oxidized glutathione in both diabetic and galactosemic rats were significantly decreased when compared to normal), overall the galactosemic rat model is not closely parallel to the diabetic rat model in extra-ocular tissues. In addition, several effects of diabetes (increased hepatic glutathione peroxidase activity, increased superoxide dismutase activity in kidney and heart, decreased renal and increased cardiac catalase activity) were not mimicked in galactosemic rats, and glutathione concentration in both liver and heart was affected in opposite ways in diabetic rats and galactose- fed rats. Insulin treatment reversed/prevented the activity changes in renal and cardiac superoxide dismutase, renal and cardiac catalase, and hepatic glutathione peroxidase as well as the hepatic changes in lipid peroxidation and reduced and oxidized glutathione, and the increase in cardiac glutathione. Thus, prudence should be exercised in the use of experimentally galactosemic rats as a model for diabetes until the correspondence of the models has been more fully characterized.

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