Please use this identifier to cite or link to this item: https://ir.swu.ac.th/jspui/handle/123456789/14856
Title: Satratoxin H generates reactive oxygen species and lipid peroxides in PC12 cells
Authors: Nusuetrong P.
Pengsuparp T.
Meksuriyen D.
Tanitsu M.
Kikuchi H.
Mizugaki M.
Shimazu K.-I.
Oshima Y.
Nakahata N.
Yoshida M.
Keywords: 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
Issue Date: 2008
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.
URI: https://ir.swu.ac.th/jspui/handle/123456789/14856
https://www.scopus.com/inward/record.uri?eid=2-s2.0-45749109056&doi=10.1248%2fbpb.31.1115&partnerID=40&md5=e1e4a9d282e4055287d49b2a3ecb96ee
ISSN: 9186158
Appears in Collections:Scopus 1983-2021

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