1. Satratoxin H generates reactive oxygen species and lipid peroxides in PC12 cells
- Author
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Masa‐aki Tanitsu, Haruhisa Kikuchi, Duangdeun Meksuriyen, Thitima Pengsuparp, Ken Ichi Shimazu, Yoshiteru Oshima, Punnee Nusuetrong, Michinao Mizugaki, Makoto Yoshida, and Norimichi Nakahata
- Subjects
Programmed cell death ,Cell Survival ,Pharmaceutical Science ,DNA Fragmentation ,Biology ,PC12 Cells ,Thiobarbituric Acid Reactive Substances ,p38 Mitogen-Activated Protein Kinases ,Antioxidants ,Lipid peroxidation ,chemistry.chemical_compound ,Animals ,Protein kinase A ,Pharmacology ,chemistry.chemical_classification ,Electrophoresis, Agar Gel ,Reactive oxygen species ,Lipid peroxide ,fungi ,G1 Phase ,JNK Mitogen-Activated Protein Kinases ,General Medicine ,Glutathione ,Malondialdehyde ,Flow Cytometry ,Cell biology ,Rats ,chemistry ,Apoptosis ,Indicators and Reagents ,Lipid Peroxidation ,Reactive Oxygen Species ,Trichothecenes - 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.
- Published
- 2008