Menadione-induced cytotoxicity to rat osteoblasts

J. S. Sun, Y. H. Tsuang, W. C. Huang, L. T. Chen, Y. S. Hang, F. J. Lu

Research output: Contribution to journalArticlepeer-review

18 Citations (Scopus)


Oxygen-derived free radical injury has been associated with several cytopathic conditions. Oxygen radicals produced by chondrocytes is an important mechanism by which chondrocytes induce matrix degradation. In the present study, we extend these observations by studying oxidative processes against osteoblasts. Osteoblasts were mixed in in vitro culture with 200 μM menadione. The cytotoxic effect of menadione-induced oxidative stress was monitored by lucigenin- or luminol-amplified chemiluminescence,tetrazolium assay and immunocytochemical study. Results showed that adding menadione induces an oxidative stress on osteoblasts, via superoxide and hydrogen peroxide production, that can be eradicated by superoxide dismutase (SOD) and catalase in a dose-dependent manner. Catalase and the appropriate concentration of dimethyl sulfoxide have a protective effect on cytotoxicity induced by menadione, whereas SOD does not. Menadione-treated osteoblasts have a strong affinity for annexin V, and the nuclei are strongly stained by TUNEL (TdT-mediated dUTP nick-end labelling). The results suggest that menadione-triggered production of reactive oxygen species leads to apoptosis of osteoblasts.

Original languageEnglish
Pages (from-to)967-976
Number of pages10
JournalCellular and Molecular Life Sciences
Issue number11-12
Publication statusPublished - 1997


  • Catalase
  • Menadione
  • Osteoblasts
  • Oxidative stress
  • Superoxide dismutase (SOD)

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology
  • Pharmacology
  • Cellular and Molecular Neuroscience
  • Cell Biology


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