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

Punnee Nusuetrong, Makoto Yoshida, Masa Aki Tanitsu, Haruhisa Kikuchi, Michinao Mizugaki, Ken Ichi Shimazu, Thitima Pengsuparp, Duangdeun Meksuriyen, Yoshiteru Oshima, Norimichi Nakahata

Research output: Contribution to journalArticlepeer-review

21 Citations (Scopus)


Satratoxins, members of the trichothecene mycotoxin family, have been known to be harmful to health. However, the mechanisms underlying the toxicity still remain unclear. The present study is undertaken to elucidate the mechanisms of the satratoxin H-induced cytotoxicity in PC12 cells. Satratoxin H caused cytotoxicity, which was reflected from apoptosis determined by chromatin staining and flow cytometry. Satratoxin H stimulated the phosphorylation of extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK). Pre-incubation with SB203580, a p38 MAPK inhibitor, or SP600125, a JNK inhibitor, but not PD98059, an ERK inhibitor, reduced satratoxin-induced cytotoxicity. Co-incubation of cells with glutathione, N-acetyl-l-cysteine or glutathione reductase inhibited cytotoxicity and the phosphorylation of p38 MAPK induced by satratoxin H. Our data suggest that satratoxin H-induced apoptosis in PC12 cells is dependent on the activation of p38 MAPK/JNK and the increase in reactive oxygen species.

Original languageEnglish
Pages (from-to)239-246
Number of pages8
JournalEuropean journal of pharmacology
Issue number1-3
Publication statusPublished - 2005 Jan 10
Externally publishedYes


  • Apoptosis
  • Glutathione
  • Mitogen-activated protein kinase
  • N-Acetyl-l-cysteine
  • Reactive oxygen species
  • Satratoxin H

ASJC Scopus subject areas

  • Pharmacology


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