Protection of LLC-PK1 cells against hydrogen peroxide-induced cell death by modulation of ceramide level

Jae Myung Yoo; Youn Sun Lee; Heon Kyo Choi; Yong Moon Lee; Jin Tae Hong; Yeo Pyo Yun; Seikwan Oh; Hwan Soo Yoo

doi:10.1007/BF02977798

Protection of LLC-PK1 cells against hydrogen peroxide-induced cell death by modulation of ceramide level

Jae Myung Yoo, Youn Sun Lee, Heon Kyo Choi, Yong Moon Lee, Jin Tae Hong, Yeo Pyo Yun, Seikwan Oh, Hwan Soo Yoo

Department of Molecular Medicine

Research output: Contribution to journal › Article › peer-review

5 Scopus citations

Abstract

Oxidative stress has been reported to elevate ceramide level during cell death. The purpose of the present study was to modulate cell death in relation to cellular glutathione (GSH) level and GST (glutathione S-transferase) expression by regulating the sphingolipid metabolism. LLC-PK1 cells were treated with H₂O₂ in the absence of serum to induce cell death. Subsequent to exposure to H₂O₂, LLC-PK1 cells were treated with desipramine, sphingomyelinase inhibitor, and N-acetylcysteine (NAC), GSH substrate. Based on comparative visual observation with H₂O ₂-treated control cells, it was observed that 0.5 μM of desipramine and 25 mM of NAC exhibited about 90 and 95% of cytoprotection, respectively, against H₂O₂-induced cell death. Desipramine and NAC lowered the release of LDH activity by 36 and 3%, respectively, when compared to 71% in H₂O₂-exposed cells. Cellular glutathione level in 500 μM H₂O₂-treated cells was reduced to 890 pmol as compared to control level of 1198 pmol per mg protein. GST P1-1 expression was decreased in H₂O₂-treated cells compared to healthy normal cells. In conclusion, it has been inferred that H₂O₂-induced cell death is closely related to cellular GSH level and GST P1-1 expression in LLC-PK1 cells and occurs via ceramide elevation by sphingomyelinase activation.

Original language	English
Pages (from-to)	311-318
Number of pages	8
Journal	Archives of Pharmacal Research
Volume	28
Issue number	3
DOIs	https://doi.org/10.1007/BF02977798
State	Published - 31 Mar 2005

Bibliographical note

Funding Information:
This work was funded by a grant from Korea Research Foundation (2002-015-EP0135).

Keywords

Cell death
Ceramide
GST
Glutathione
LLC-PK1 cells

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title = "Protection of LLC-PK1 cells against hydrogen peroxide-induced cell death by modulation of ceramide level",

abstract = "Oxidative stress has been reported to elevate ceramide level during cell death. The purpose of the present study was to modulate cell death in relation to cellular glutathione (GSH) level and GST (glutathione S-transferase) expression by regulating the sphingolipid metabolism. LLC-PK1 cells were treated with H2O2 in the absence of serum to induce cell death. Subsequent to exposure to H2O2, LLC-PK1 cells were treated with desipramine, sphingomyelinase inhibitor, and N-acetylcysteine (NAC), GSH substrate. Based on comparative visual observation with H2O 2-treated control cells, it was observed that 0.5 μM of desipramine and 25 mM of NAC exhibited about 90 and 95% of cytoprotection, respectively, against H2O2-induced cell death. Desipramine and NAC lowered the release of LDH activity by 36 and 3%, respectively, when compared to 71% in H2O2-exposed cells. Cellular glutathione level in 500 μM H2O2-treated cells was reduced to 890 pmol as compared to control level of 1198 pmol per mg protein. GST P1-1 expression was decreased in H2O2-treated cells compared to healthy normal cells. In conclusion, it has been inferred that H2O2-induced cell death is closely related to cellular GSH level and GST P1-1 expression in LLC-PK1 cells and occurs via ceramide elevation by sphingomyelinase activation.",

keywords = "Cell death, Ceramide, GST, Glutathione, LLC-PK1 cells",

author = "Yoo, {Jae Myung} and Lee, {Youn Sun} and Choi, {Heon Kyo} and Lee, {Yong Moon} and Hong, {Jin Tae} and Yun, {Yeo Pyo} and Seikwan Oh and Yoo, {Hwan Soo}",

note = "Funding Information: This work was funded by a grant from Korea Research Foundation (2002-015-EP0135).",

year = "2005",

month = mar,

day = "31",

doi = "10.1007/BF02977798",

language = "English",

volume = "28",

pages = "311--318",

journal = "Archives of Pharmacal Research",

issn = "0253-6269",

publisher = "Pharmaceutical Society of Korea",

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T1 - Protection of LLC-PK1 cells against hydrogen peroxide-induced cell death by modulation of ceramide level

AU - Yoo, Jae Myung

AU - Lee, Youn Sun

AU - Choi, Heon Kyo

AU - Lee, Yong Moon

AU - Hong, Jin Tae

AU - Yun, Yeo Pyo

AU - Oh, Seikwan

AU - Yoo, Hwan Soo

N1 - Funding Information: This work was funded by a grant from Korea Research Foundation (2002-015-EP0135).

PY - 2005/3/31

Y1 - 2005/3/31

N2 - Oxidative stress has been reported to elevate ceramide level during cell death. The purpose of the present study was to modulate cell death in relation to cellular glutathione (GSH) level and GST (glutathione S-transferase) expression by regulating the sphingolipid metabolism. LLC-PK1 cells were treated with H2O2 in the absence of serum to induce cell death. Subsequent to exposure to H2O2, LLC-PK1 cells were treated with desipramine, sphingomyelinase inhibitor, and N-acetylcysteine (NAC), GSH substrate. Based on comparative visual observation with H2O 2-treated control cells, it was observed that 0.5 μM of desipramine and 25 mM of NAC exhibited about 90 and 95% of cytoprotection, respectively, against H2O2-induced cell death. Desipramine and NAC lowered the release of LDH activity by 36 and 3%, respectively, when compared to 71% in H2O2-exposed cells. Cellular glutathione level in 500 μM H2O2-treated cells was reduced to 890 pmol as compared to control level of 1198 pmol per mg protein. GST P1-1 expression was decreased in H2O2-treated cells compared to healthy normal cells. In conclusion, it has been inferred that H2O2-induced cell death is closely related to cellular GSH level and GST P1-1 expression in LLC-PK1 cells and occurs via ceramide elevation by sphingomyelinase activation.

AB - Oxidative stress has been reported to elevate ceramide level during cell death. The purpose of the present study was to modulate cell death in relation to cellular glutathione (GSH) level and GST (glutathione S-transferase) expression by regulating the sphingolipid metabolism. LLC-PK1 cells were treated with H2O2 in the absence of serum to induce cell death. Subsequent to exposure to H2O2, LLC-PK1 cells were treated with desipramine, sphingomyelinase inhibitor, and N-acetylcysteine (NAC), GSH substrate. Based on comparative visual observation with H2O 2-treated control cells, it was observed that 0.5 μM of desipramine and 25 mM of NAC exhibited about 90 and 95% of cytoprotection, respectively, against H2O2-induced cell death. Desipramine and NAC lowered the release of LDH activity by 36 and 3%, respectively, when compared to 71% in H2O2-exposed cells. Cellular glutathione level in 500 μM H2O2-treated cells was reduced to 890 pmol as compared to control level of 1198 pmol per mg protein. GST P1-1 expression was decreased in H2O2-treated cells compared to healthy normal cells. In conclusion, it has been inferred that H2O2-induced cell death is closely related to cellular GSH level and GST P1-1 expression in LLC-PK1 cells and occurs via ceramide elevation by sphingomyelinase activation.

KW - Cell death

KW - Ceramide

KW - GST

KW - Glutathione

KW - LLC-PK1 cells

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DO - 10.1007/BF02977798

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SN - 0253-6269

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JO - Archives of Pharmacal Research

JF - Archives of Pharmacal Research

IS - 3

ER -

Protection of LLC-PK1 cells against hydrogen peroxide-induced cell death by modulation of ceramide level

Abstract

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Keywords

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