Involvement of mitochondrial alteration and reactive oxygen species generation in Taiwan cobra cardiotoxin-induced apoptotic death of human neuroblastoma SK-N-SH cells

Ku Chung Chen, Shinne Ren Lin, Long Sen Chang

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Naja naja atra cardiotoxin 3 (CTX3) induced apoptotic death on human neuroblastoma SK-N-SH cells. The apoptosis signals of CTX3 included reactive oxygen species (ROS) generation, disruption of mitochondrial membrane potential (ΔΨm), cytochrome c release to the cytosol and activation of caspase-9 and -3. However, CTX3-induced increase in mitochondrial permeability transition was not initiated by proteins of the Bcl-2 family. The collapse of ΔΨm, release of cytosolic cytochrome c, production of ROS and subsequent apoptotic cell death in CTX-treated cells could not be completely abolished by either N-acetylcysteine (ROS scavenger) or cyclosporin A (an inhibitor of mitochondrial permeability transition). Co-incubation with rotenone, an inhibitor of mitochondrial electron transport chain complexes I, resulted in partial inhibition of CTX3-induced ROS generation but not the loss of ΔΨm. Obviously, the dissipation of ΔΨm was not an upstream event for ROS generation or vice versa. Given that CTX3 was able to induce the leakage of isolated mitochondria, our data indicate that CTX3-induced apoptotic death of SK-N-SH cells is mediated through mitochondrial alteration and ROS generation.

Original languageEnglish
Pages (from-to)361-368
Number of pages8
JournalToxicon
Volume52
Issue number2
DOIs
Publication statusPublished - Aug 1 2008
Externally publishedYes

Keywords

  • Cardiotoxin
  • Cytotoxicity
  • Mitochondrial alteration
  • Reactive oxygen species generation

ASJC Scopus subject areas

  • Toxicology

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