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Resistance to H2O2-induced oxidative stress in human cells of different phenotypes. / Zenin, Valeriy; Ivanova, Julia; Pugovkina, Natalia; Shatrova, Alla; Aksenov, Nikolay; Tyuryaeva, Irina; Kirpichnikova, Kseniya; Kuneev, Ivan; Zhuravlev, Andrei; Osyaeva, Ekaterina; Lyublinskaya, Ekaterina; Gazizova, Ilyuza; Guriev, Nikita; Lyublinskaya, Olga.

In: Redox Biology, Vol. 50, No. 102245, 102245, 01.04.2022.

Research output: Contribution to journalArticlepeer-review

Harvard

Zenin, V, Ivanova, J, Pugovkina, N, Shatrova, A, Aksenov, N, Tyuryaeva, I, Kirpichnikova, K, Kuneev, I, Zhuravlev, A, Osyaeva, E, Lyublinskaya, E, Gazizova, I, Guriev, N & Lyublinskaya, O 2022, 'Resistance to H2O2-induced oxidative stress in human cells of different phenotypes', Redox Biology, vol. 50, no. 102245, 102245. https://doi.org/10.1016/j.redox.2022.102245

APA

Zenin, V., Ivanova, J., Pugovkina, N., Shatrova, A., Aksenov, N., Tyuryaeva, I., Kirpichnikova, K., Kuneev, I., Zhuravlev, A., Osyaeva, E., Lyublinskaya, E., Gazizova, I., Guriev, N., & Lyublinskaya, O. (2022). Resistance to H2O2-induced oxidative stress in human cells of different phenotypes. Redox Biology, 50(102245), [102245]. https://doi.org/10.1016/j.redox.2022.102245

Vancouver

Zenin V, Ivanova J, Pugovkina N, Shatrova A, Aksenov N, Tyuryaeva I et al. Resistance to H2O2-induced oxidative stress in human cells of different phenotypes. Redox Biology. 2022 Apr 1;50(102245). 102245. https://doi.org/10.1016/j.redox.2022.102245

Author

Zenin, Valeriy ; Ivanova, Julia ; Pugovkina, Natalia ; Shatrova, Alla ; Aksenov, Nikolay ; Tyuryaeva, Irina ; Kirpichnikova, Kseniya ; Kuneev, Ivan ; Zhuravlev, Andrei ; Osyaeva, Ekaterina ; Lyublinskaya, Ekaterina ; Gazizova, Ilyuza ; Guriev, Nikita ; Lyublinskaya, Olga. / Resistance to H2O2-induced oxidative stress in human cells of different phenotypes. In: Redox Biology. 2022 ; Vol. 50, No. 102245.

BibTeX

@article{8f8367c1fe4d48d18d123244af3209c4,
title = "Resistance to H2O2-induced oxidative stress in human cells of different phenotypes",
abstract = "Application of genetically encoded biosensors of redox-active compounds promotes the elaboration of new methods for investigation of intracellular redox activities. Previously, we have developed a method to measure quantitatively the intracellular concentration of hydrogen peroxide (H2O2) in living cells using genetically encoded biosensor HyPer. In the present study, we refined the method and applied it for comparing the antioxidant system potency in human cells of different phenotypes by measuring the gradient between the extracellular and cytoplasmic H2O2 concentrations under conditions of H2O2-induced external oxidative stress. The measurements were performed using cancer cell lines (K-562 and HeLa), as well as normal human cells – all expressing HyPer in the cell cytoplasm. As normal cells, we used three isogenic lines of different phenotypes – mesenchymal stem/stromal cells (MSCs), induced pluripotent stem cells (iPSCs) derived from MSCs by reprogramming, and differentiated iPSC progenies with the phenotype resembling precursory MSCs. When exposing cells to exogenous H2O2, we showed that at low oxidative loads (<50 μM of H2O2) the gradient depended on extracellular H2O2 concentration. At high loads (>50 μM of H2O2), which caused the exhaustion of thioredoxin activity in the cell cytoplasm, the gradient stabilized, pointing out that it is the functional status of the thioredoxin-depended enzymatic system that drives the dependence of the H2O2 gradient on the oxidative load in human cells. At high H2O2 concentrations, the cytoplasmic H2O2 level in cancer cells was found to be several hundred times lower than the extracellular one. At the same time, in normal cells, extracellular-to-intracellular gradient amounted to thousands of times. Upon reprogramming, the potency of cellular antioxidant defense increased. In contrast, differentiation of iPSCs did not result in the changes in antioxidant system activity in the cell cytoplasm, assuming that intensification of the H2O2-detoxification processes is inherent to a period of early human development.",
keywords = "Cell reprogramming, Genetically encoded biosensors, HO, HO gradient, Hydrogen peroxide, HyPer, Induced pluripotent stem cells, Kinetics, Mesenchymal stem/stromal cells, Rate constants, Oxidative Stress, Hydrogen Peroxide/metabolism, Humans, Mesenchymal Stem Cells/metabolism, Phenotype, HeLa Cells, H2O2, H2O2 gradient",
author = "Valeriy Zenin and Julia Ivanova and Natalia Pugovkina and Alla Shatrova and Nikolay Aksenov and Irina Tyuryaeva and Kseniya Kirpichnikova and Ivan Kuneev and Andrei Zhuravlev and Ekaterina Osyaeva and Ekaterina Lyublinskaya and Ilyuza Gazizova and Nikita Guriev and Olga Lyublinskaya",
note = "Publisher Copyright: {\textcopyright} 2022 The Authors",
year = "2022",
month = apr,
day = "1",
doi = "10.1016/j.redox.2022.102245",
language = "English",
volume = "50",
journal = "Redox Biology",
issn = "2213-2317",
publisher = "Elsevier",
number = "102245",

}

RIS

TY - JOUR

T1 - Resistance to H2O2-induced oxidative stress in human cells of different phenotypes

AU - Zenin, Valeriy

AU - Ivanova, Julia

AU - Pugovkina, Natalia

AU - Shatrova, Alla

AU - Aksenov, Nikolay

AU - Tyuryaeva, Irina

AU - Kirpichnikova, Kseniya

AU - Kuneev, Ivan

AU - Zhuravlev, Andrei

AU - Osyaeva, Ekaterina

AU - Lyublinskaya, Ekaterina

AU - Gazizova, Ilyuza

AU - Guriev, Nikita

AU - Lyublinskaya, Olga

N1 - Publisher Copyright: © 2022 The Authors

PY - 2022/4/1

Y1 - 2022/4/1

N2 - Application of genetically encoded biosensors of redox-active compounds promotes the elaboration of new methods for investigation of intracellular redox activities. Previously, we have developed a method to measure quantitatively the intracellular concentration of hydrogen peroxide (H2O2) in living cells using genetically encoded biosensor HyPer. In the present study, we refined the method and applied it for comparing the antioxidant system potency in human cells of different phenotypes by measuring the gradient between the extracellular and cytoplasmic H2O2 concentrations under conditions of H2O2-induced external oxidative stress. The measurements were performed using cancer cell lines (K-562 and HeLa), as well as normal human cells – all expressing HyPer in the cell cytoplasm. As normal cells, we used three isogenic lines of different phenotypes – mesenchymal stem/stromal cells (MSCs), induced pluripotent stem cells (iPSCs) derived from MSCs by reprogramming, and differentiated iPSC progenies with the phenotype resembling precursory MSCs. When exposing cells to exogenous H2O2, we showed that at low oxidative loads (<50 μM of H2O2) the gradient depended on extracellular H2O2 concentration. At high loads (>50 μM of H2O2), which caused the exhaustion of thioredoxin activity in the cell cytoplasm, the gradient stabilized, pointing out that it is the functional status of the thioredoxin-depended enzymatic system that drives the dependence of the H2O2 gradient on the oxidative load in human cells. At high H2O2 concentrations, the cytoplasmic H2O2 level in cancer cells was found to be several hundred times lower than the extracellular one. At the same time, in normal cells, extracellular-to-intracellular gradient amounted to thousands of times. Upon reprogramming, the potency of cellular antioxidant defense increased. In contrast, differentiation of iPSCs did not result in the changes in antioxidant system activity in the cell cytoplasm, assuming that intensification of the H2O2-detoxification processes is inherent to a period of early human development.

AB - Application of genetically encoded biosensors of redox-active compounds promotes the elaboration of new methods for investigation of intracellular redox activities. Previously, we have developed a method to measure quantitatively the intracellular concentration of hydrogen peroxide (H2O2) in living cells using genetically encoded biosensor HyPer. In the present study, we refined the method and applied it for comparing the antioxidant system potency in human cells of different phenotypes by measuring the gradient between the extracellular and cytoplasmic H2O2 concentrations under conditions of H2O2-induced external oxidative stress. The measurements were performed using cancer cell lines (K-562 and HeLa), as well as normal human cells – all expressing HyPer in the cell cytoplasm. As normal cells, we used three isogenic lines of different phenotypes – mesenchymal stem/stromal cells (MSCs), induced pluripotent stem cells (iPSCs) derived from MSCs by reprogramming, and differentiated iPSC progenies with the phenotype resembling precursory MSCs. When exposing cells to exogenous H2O2, we showed that at low oxidative loads (<50 μM of H2O2) the gradient depended on extracellular H2O2 concentration. At high loads (>50 μM of H2O2), which caused the exhaustion of thioredoxin activity in the cell cytoplasm, the gradient stabilized, pointing out that it is the functional status of the thioredoxin-depended enzymatic system that drives the dependence of the H2O2 gradient on the oxidative load in human cells. At high H2O2 concentrations, the cytoplasmic H2O2 level in cancer cells was found to be several hundred times lower than the extracellular one. At the same time, in normal cells, extracellular-to-intracellular gradient amounted to thousands of times. Upon reprogramming, the potency of cellular antioxidant defense increased. In contrast, differentiation of iPSCs did not result in the changes in antioxidant system activity in the cell cytoplasm, assuming that intensification of the H2O2-detoxification processes is inherent to a period of early human development.

KW - Cell reprogramming

KW - Genetically encoded biosensors

KW - HO

KW - HO gradient

KW - Hydrogen peroxide

KW - HyPer

KW - Induced pluripotent stem cells

KW - Kinetics

KW - Mesenchymal stem/stromal cells

KW - Rate constants

KW - Oxidative Stress

KW - Hydrogen Peroxide/metabolism

KW - Humans

KW - Mesenchymal Stem Cells/metabolism

KW - Phenotype

KW - HeLa Cells

KW - H2O2

KW - H2O2 gradient

UR - http://www.scopus.com/inward/record.url?scp=85123742039&partnerID=8YFLogxK

UR - https://www.mendeley.com/catalogue/a42ea648-00c1-352d-9178-2ed0afcbc5dd/

U2 - 10.1016/j.redox.2022.102245

DO - 10.1016/j.redox.2022.102245

M3 - Article

C2 - 35114579

AN - SCOPUS:85123742039

VL - 50

JO - Redox Biology

JF - Redox Biology

SN - 2213-2317

IS - 102245

M1 - 102245

ER -

ID: 98153940