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Involvement of reactive oxygen species and stress-activated MAPKs in satratoxin H-induced apoptosis

Punnee Nusuetrong1, Makoto Yoshida, Masa-aki Tanitsu

  • 1Department of Cellular Signaling, Graduate School of Pharmaceutical Sciences, Tohoku University, 6-3 Aoba, Aramaki, Aoba-ku, Sendai 980-8578, Japan.

European Journal of Pharmacology
|January 22, 2005
PubMed

Insights

Satratoxin H triggers cell death (cytotoxicity) by causing apoptosis in PC12 cells. This process involves the activation of p38 MAPK/JNK pathways and increased reactive oxygen species.

Area of Science:

  • Toxicology
  • Cell Biology
  • Biochemistry

Background:

  • Satratoxins are trichothecene mycotoxins with known health risks.
  • The precise mechanisms of satratoxin toxicity are not fully understood.

Purpose of the Study:

  • To investigate the mechanisms of satratoxin H-induced cytotoxicity in PC12 cells.
  • To elucidate the role of specific signaling pathways and oxidative stress.

Main Methods:

  • Assessing cytotoxicity and apoptosis via chromatin staining and flow cytometry.
  • Analyzing the phosphorylation of extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK).
  • Evaluating the effects of pathway inhibitors (SB203580, SP600125, PD98059) and antioxidants (glutathione, N-acetyl-L-cysteine, glutathione reductase).

Main Results:

  • Satratoxin H induced apoptosis and cytotoxicity in PC12 cells.
  • Satratoxin H activated p38 MAPK and JNK pathways, but not ERK.
  • Inhibitors of p38 MAPK/JNK and antioxidants reduced satratoxin H-induced cytotoxicity and p38 MAPK phosphorylation.

Conclusions:

  • Satratoxin H-induced apoptosis in PC12 cells is mediated by p38 MAPK and JNK activation.
  • Increased reactive oxygen species play a critical role in satratoxin H toxicity.

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