Reactive oxygen species induce cardiomyocyte apoptosis partly through TNF-alpha

Cytokine. 2002 May 21;18(4):179-83. doi: 10.1006/cyto.2001.1007.


Many studies have indicated that oxidative stress induces apoptosis in cardiomyocytes, but its mechanism remains unknown. We examined whether tumor necrosis factor-alpha (TNF-alpha) is involved in oxidative stress-induced cardiomyocyte apoptosis. Pretreatment with anti-TNF-alpha antibody significantly decreased the number of H(2)O(2)-induced TUNEL-positive cardiomyocytes. Expression of TNF-alpha gene was upregulated by H(2)O(2), and H(2)O(2) mildly but significantly increased the concentration of TNF-alpha in the culture medium. Although neither low dose of H(2)O(2) nor TNF-alpha induced apoptosis, stimulation with H(2)O(2) and TNF-alpha synergistically increased apoptosis. These results suggest that oxidative stress induces apoptosis of cardiac myocytes partly through TNF-alpha.

MeSH terms

  • Animals
  • Animals, Newborn
  • Apoptosis*
  • Cells, Cultured
  • Hydrogen Peroxide / pharmacology
  • In Situ Nick-End Labeling
  • Myocardium / cytology
  • Myocardium / pathology*
  • Oxidative Stress
  • Rats
  • Rats, Wistar
  • Reactive Oxygen Species*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Time Factors
  • Tumor Necrosis Factor-alpha / metabolism*
  • Up-Regulation


  • Reactive Oxygen Species
  • Tumor Necrosis Factor-alpha
  • Hydrogen Peroxide