Effects of Lead and Cadmium on Brain Endothelial Cell Survival, Monolayer Permeability, and Crucial Oxidative Stress Markers in an in Vitro Model of the Blood-Brain Barrier

Abstract Background: Although cardioplegia is used since the ‘70s of the last century, debate on cardioprotection during cardio-surgical procedures is still actual. The selection of a particular method depends mainly on the preferences and experience of a specific center or even surgeon. Crystalloid cardioplegia is an aqueous ion solution similar to intracellular (Custodiol HTK) or extracellular (Plegisol) fluid. Numerous publications compare different types of cardioplegic solutions, but only a few used cultured cells in laboratory conditions. Methods: In this study, the authors compare two crystalloid solutions using an in-vitro model simulating cardioplegic arrest. The efficacy of myocardial protection during ischemia was investigated with susceptible indicators like the appearance of the deleterious effect of reactive oxygen species and oxidative stress markers. Incubated human cardiomyocytes and rat cardiomyoblasts H9C2 in cardioplegia for 4h were examined for expression of oxidative stress markers (MnSOD, iNOS, HSP27), cardioplegic solutions cytotoxicity, and peroxidation damage of the cell’s lipids and proteins. All tests were performed after 0.5h, 1h, 2h, and 4h in identical physical and biological conditions, which is difficult to achieve in clinical trials. Results: The tests performed on matured cells of human cardiomyocytes showed the superiority of Custodiol HTK. Differences between solutions on immature cells H9C2 were not relevant. Both Plegisol and Custodiol HTK produced a similar expression of MnSOD and iNOS. There was no significant advantage of Custodiol over Plegisol in the cytotoxicity test. However, Custodiol induced a higher level of lipid peroxidation. Conclusions: Considering proceeded examinations on cultured cardiomyocytes, Custodiol HTK appears to be safer than Plegisol.

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Measurement of Oxidative Stress Markers In Vitro Using Commercially Available Kits

Measuring Oxidants and Oxidative Stress in Biological Systems - Biological Magnetic Resonance ◽

10.1007/978-3-030-47318-1_4 ◽

2020 ◽

pp. 39-60 ◽

Cited By ~ 1

Author(s):

Bryan Gardiner ◽

Julie A. Dougherty ◽

Devasena Ponnalagu ◽

Harpreet Singh ◽

Mark Angelos ◽

...

Keyword(s):

Oxidative Stress ◽

Oxidative Stress Markers ◽

Stress Markers

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Estimation of the Genotoxicityof Hydrogen Peroxide and Antioxidant Actionof Halo Acid by the Method of Dna-Cometwith the Use of the Model of Transplantable Cell Cultures

Vestnik Volgogradskogo Gosudarstvennogo Universiteta Serija 11 Estestvennye nauki ◽

10.15688/jvolsu11.2018.1.7 ◽

2018 ◽

pp. 40-43

Author(s):

Olga Verle ◽

Oleg Ostrovskiy ◽

Valerian Verovskiy ◽

Galina Dudchenko

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

In Vitro Model ◽

Cell Damage ◽

Protective Action ◽

Genetic Material ◽

Optimal Level ◽

Pharmacological Agents ◽

Vitro Model

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.

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Isoflurane preconditioning inhibits the effects of tissue-type plasminogen activator on brain endothelial cell in an in vitro model of ischemic stroke

International Journal of Medical Sciences ◽

10.7150/ijms.18037 ◽

2017 ◽

Vol 14 (5) ◽

pp. 425-433 ◽

Cited By ~ 10

Author(s):

So Yeong Cheon ◽

So Yeon Kim ◽

Eun Hee Kam ◽

Jae Hoon Lee ◽

Jeong Min Kim ◽

...

Keyword(s):

Ischemic Stroke ◽

Endothelial Cell ◽

Plasminogen Activator ◽

In Vitro Model ◽

Tissue Type ◽

Brain Endothelial Cell ◽

Tissue Type Plasminogen Activator ◽

Type Plasminogen Activator ◽

Vitro Model

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In vitro effect of vanadyl sulfate on cultured primary astrocytes: cell viability and oxidative stress markers.

Journal of Applied Toxicology ◽

10.1002/jat.3939 ◽

2020 ◽

Vol 40 (6) ◽

pp. 737-747

Author(s):

Agnieszka Ścibior ◽

Konrad A. Szychowski ◽

Iwona Zwolak ◽

Klaudia Dachowska ◽

Jan Gmiński

Keyword(s):

Oxidative Stress ◽

Cell Viability ◽

Vanadyl Sulfate ◽

Oxidative Stress Markers ◽

Stress Markers ◽

Primary Astrocytes ◽

Vitro Effect ◽

And Oxidative Stress

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2-Hydroxy-(4-methylseleno)butanoic Acid Is Used by Intestinal Caco-2 Cells as a Source of Selenium and Protects against Oxidative Stress

Journal of Nutrition ◽

10.1093/jn/nxz190 ◽

2019 ◽

Vol 149 (12) ◽

pp. 2191-2198

Author(s):

Joan Campo-Sabariz ◽

David Moral-Anter ◽

M Teresa Brufau ◽

Mickael Briens ◽

Eric Pinloche ◽

...

Keyword(s):

Oxidative Stress ◽

In Vitro Model ◽

Thioredoxin Reductase ◽

Protein Carbonyl ◽

Butanoic Acid ◽

H2o2 Treatment ◽

Vitro Model ◽

Gpx Activity

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.

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