Publication:
Satratoxin H generates reactive oxygen species and lipid peroxides in PC12 cells

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Issued Date

2008

Resource Type

Article

File Type

application/pdf

ISSN

9186158

DOI

10.1248/bpb.31.1115

Other identifier(s)

2-s2.0-45749109056

Rights Holder(s)

มหาวิทยาลัยศรีนครินทรวิโรฒ

Bibliographic Citation

Biological and Pharmaceutical Bulletin. Vol 31, No.6 (2008), p.1115-1120

Suggested Citation

Nusuetrong P., Pengsuparp T., Meksuriyen D., Tanitsu M., Kikuchi H., Mizugaki M., Shimazu K.-I., Oshima Y., Nakahata N., Yoshida M. Satratoxin H generates reactive oxygen species and lipid peroxides in PC12 cells. Biological and Pharmaceutical Bulletin. Vol 31, No.6 (2008), p.1115-1120. doi:10.1248/bpb.31.1115 Retrieved from: https://hdl.handle.net/20.500.14740/4020

Title

Satratoxin H generates reactive oxygen species and lipid peroxides in PC12 cells

Author(s)

Nusuetrong P.
 Pengsuparp T.
 Meksuriyen D.
 Tanitsu M.
 Kikuchi H.
 Mizugaki M.
 Shimazu K.-I.
 Oshima Y.
 Nakahata N.
 Yoshida M.

Abstract

Satratoxin H, a mycotoxin, is thought to induce apoptosis of PC12 cells through the activation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK) in a glutathione (GSH)-sensitive manner. The present study was undertaken to further elucidate the mechanism by which satratoxin H induces cell death in PC12 cells. Satratoxin H caused apoptosis of PC12 cells within 24-h, as determined by DNA fragmentation and flow cytometric analysis. Satratoxin H increased reactive oxygen species (ROS) production and lipid peroxidation, as determined by malondialdehyde formation. These effects were attenuated by incubation of cells with GSH, suggesting that satratoxin H-induced increase in apoptosis of serum-deprived PC12 cells may be partially mediated through the generation of ROS. © 2008 Pharmaceutical Society of Japan.

Subject(s)

Glutathione
 Lipid peroxide
 Malonaldehyde
 Mycotoxin
 Reactive oxygen metabolite
 Satratoxin h
 Animal cell
 Apoptosis
 Article
 Cell viability
 Controlled study
 DNA fragmentation
 Drug effect
 Drug mechanism
 Flow cytometry
 Lipid peroxidation
 Nonhuman
 Pheochromocytoma
 Rat
 Animals
 Antioxidants
 Cell Survival
 DNA Fragmentation
 Electrophoresis, Agar Gel
 Flow Cytometry
 G1 Phase
 Glutathione
 Indicators and Reagents
 JNK Mitogen-Activated Protein Kinases
 Lipid Peroxidation
 P38 Mitogen-Activated Protein Kinases
 PC12 Cells
 Rats
 Reactive Oxygen Species
 Thiobarbituric Acid Reactive Substances
 Trichothecenes

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URI

https://hdl.handle.net/20.500.14740/4020

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Scopus: Year 1983-2021

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