scholarly journals An Insight into Sargassum muticum Cytoprotective Mechanisms against Oxidative Stress on a Human Cell In Vitro Model

Marine Drugs ◽  
2017 ◽  
Vol 15 (11) ◽  
pp. 353 ◽  
Author(s):  
Susete Pinteus ◽  
Marco Lemos ◽  
Joana Silva ◽  
Celso Alves ◽  
Agnieszka Neugebauer ◽  
...  
2015 ◽  
Vol 238 (2) ◽  
pp. S345-S346
Author(s):  
A. Anadón ◽  
M. Martínez ◽  
I. Ares ◽  
E. Ramos ◽  
V. Castellano ◽  
...  

Author(s):  
Olga Verle ◽  
Oleg Ostrovskiy ◽  
Valerian Verovskiy ◽  
Galina Dudchenko

In the framework of the study, the degree of defragmentation of DNA by the DNA-comet method is evaluated when exposed to the cell culture of hydrogen peroxide (H2O2), and an in vitro model is developed to evaluate the antioxidant activity of new pharmacological agents. The results of working with cell lines show that the percentage of damage to the genetic material of cells of intact samples does not greatly vary from the method of removing the cellular monolayer from the culture plastic. Concerning the effect of H2O2 as an inducer of oxidative stress on DNA cell damage, the optimal level of DNA defragmentation has been modeled for subsequent studies of the protective action of antioxidants.


2019 ◽  
Vol 149 (12) ◽  
pp. 2191-2198
Author(s):  
Joan Campo-Sabariz ◽  
David Moral-Anter ◽  
M Teresa Brufau ◽  
Mickael Briens ◽  
Eric Pinloche ◽  
...  

ABSTRACT Background Selenium (Se) participates in different functions in humans and other animals through its incorporation into selenoproteins as selenocysteine. Inadequate dietary Se is considered a risk factor for several chronic diseases associated with oxidative stress. Objective The role of 2-hydroxy-(4-methylseleno)butanoic acid (HMSeBA), an organic form of Se used in animal nutrition, in supporting selenoprotein synthesis and protecting against oxidative stress was investigated in an in vitro model of intestinal Caco-2 cells. Methods Glutathione peroxidase (GPX) and thioredoxin reductase (TXNRD) activities, selenoprotein P1 protein (SELENOP) and gene (SELENOP) expression, and GPX1 and GPX2 gene expression were studied in Se-deprived (FBS removal) and further HMSeBA-supplemented (0.1–625 μM, 72 h) cultures. The effect of HMSeBA supplementation (12.5 and 625 μM, 24 h) on oxidative stress induced by H2O2 (1 mM) was evaluated by the production of reactive oxygen species (ROS), 4-hydroxy-2-nonenal (4-HNE) adducts, and protein carbonyl residues compared with a sodium selenite control (SS, 5 μM). Results Se deprivation induced a reduction (P < 0.05) in GPX activity (62%), GPX1 expression, and both SELENOP (33%) and SELENOP expression. In contrast, an increase (P < 0.05) in GPX2 expression and no effect in TXNRD activity (P = 0.09) were observed. HMSeBA supplementation increased (P < 0.05) GPX activity (12.5–625 μM, 1.68–1.82-fold) and SELENOP protein expression (250 and 625 μM, 1.87- and 2.04-fold). Moreover, HMSeBA supplementation increased (P < 0.05) GPX1 (12.5 and 625 μM), GPX2 (625 μM), and SELENOP (12.5 and 625 μM) expression. HMSeBA (625 μM) was capable of decreasing (P < 0.05) ROS (32%), 4-HNE adduct (49%), and protein carbonyl residue (75%) production after H2O2 treatment. Conclusion Caco-2 cells can use HMSeBA as an Se source for selenoprotein synthesis, resulting in protection against oxidative stress.


PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0120485 ◽  
Author(s):  
Hans Vergauwen ◽  
Bart Tambuyzer ◽  
Karen Jennes ◽  
Jeroen Degroote ◽  
Wei Wang ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Chang Liu ◽  
Bozhao Li ◽  
Qi Yan ◽  
Shaopeng Niu ◽  
Yiding Zhao ◽  
...  

Ischemic heart disease (IHD) is a cardiovascular disease with high fatality rate, and its pathogenesis is closely related to oxidative stress. Reactive oxygen species (ROS) in oxidative stress can lead to myocardial ischemia (MI) injury in many ways. Therefore, the application of antioxidants may be an effective way to prevent IHD. In recent years, glutathione peroxidase 4 (GPx4) has received increasing attention due to its antioxidant effect. In a previous study, we used the new chimeric tRNAUTuT6 to express highly active recombinant human GPx4 (rhGPx4) in amber-less Escherichia coli. In this study, we established an isoproterenol- (ISO-) induced MI injury model in rats and an in vitro model to research the protective effect and mechanism of rhGPx4 on MI injury. The results showed that rhGPx4 could reduce the area of myocardial infarction and ameliorate the pathological injury of heart tissue, significantly reduce ISO-induced abnormalities on electrocardiogram (ECG) and cardiac serum biomarkers, protect mitochondrial function, and attenuate cardiac oxidative stress injury. In an in vitro model, the results also confirmed that rhGPx4 could inhibit ISO-induced oxidative stress injury and cardiomyocyte apoptosis. The mechanism of action of rhGPx4 involves not only the inhibition of lipid peroxidation by eliminating ROS but also keeping a normal level of endogenous antioxidant enzymes by eliminating ROS, thereby preventing oxidative stress injury in cardiomyocytes. Additionally, rhGPx4 could inhibit cardiomyocyte apoptosis through a mitochondria-dependent pathway. In short, rhGPx4, a recombinant antioxidant enzyme, can play an important role in the prevention of IHD and may have great potential for application.


2021 ◽  
Vol 18 (2) ◽  
pp. 33-37
Author(s):  
M. B. Monguno ◽  
E. S. Philip ◽  
I. C. Uku ◽  
I. O. Igbokwe

Under conditions of oxidative stress, erythrocytes of goats could be predisposed to haemolysis. This study was aimed at evaluating the effect of oxidant exposure to goat erythrocytes using an in vitro model. Blood samples from 10 goats were incubated with 0.06 – 0.18 mM hydrogen peroxide (H2O2) either singly or in combination with 0.02 µM dexamethasone for 60 min, and erythrocyte parameters such as packed cell volume (PCV), red blood cell count (RBC), mean corpuscular volume (MCV) and percentage haemolysis in hypotonic sucrose solution (250 mOsmol/L) were determined thereafter. No significant changes in the mean values of all parameters were observed. The in vitro model indicated that erythrocyte parameters remained stable under low-grade oxidant exposure in goats. Therefore, plasma H2O2 concentration of ≤ 0.18 mM, whether in the presence or absence of 0.02 µM dexamethasone, may not induce apparent oxidative damage in goat erythrocytes that could be estimated by PCV, RBC, MCV and sucrose-based osmotic fragility at low hypotonicity.


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