Reactive oxygen species are crucial for hydroxychavicol toxicity toward KB epithelial cells

J. H. Jeng, Y. J. Wang, W. H. Chang, H. L. Wu, C. H. Li, B. J. Uang, J. J. Kang, J. J. Lee, L. J. Hahn, B. R. Lin, M. C. Chang

Research output: Contribution to journalArticle

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Abstract

Betel quid (BQ) chewing shows a strong correlation to the incidence of oral submucous fibrosis (OSF), leukoplakia and oral cancer. BQ contains mainly areca nut, lime, Piper betle leaf (PBL) and the inflorescence of P. betle (IPB). Hydroxychavicol (4-allyl-catechol, HC), as a major phenolic compound in PBL and IPB, is shown to induce oxidative stress, glutathione (GSH) depletion and cell cycle deregulation. Using bivariate BrdU/PI flow cytometry, KB cells in DNA synthesis (S phase) are shown to be sensitive to the toxic effect of HC and show cell cycle arrest and apoptosis following exposure to 0.1 and 0.3 mM HC. HC-induced apoptosis and cell cycle arrest are associated with mitochondrial membrane potential (Δψm) depolarization as revealed by a decrease in rhodamine fluorescence. N-acetyl-L-cysteine (1 mM), superoxide dismutase (100 U/ml) and catalase (1000 U/ml) were effective in prevention of HC-induced GSH depletion (as indicated by chloromethylfluorescein fluorescence), reactive oxygen species (ROS) production (by dichlorofluorescein fluorescence), cell cycle arrest and apoptosis. However, dimethylthiourea (2 mM), neocuproine (1 mM), 1,10-phenanthroline (200 μM) and desferrioxamine (0.5 mM) showed little effect on HC-induced cell changes. HC elevated the cellular and mitochondrial GSH levels at moderate concentrations (0.05-0.1 mM), whereas at a concentration of 0.3 mM, inhibitory effects were noted. These results indicate that HC consumption may be associated with BQ-chewing-related oral mucosal diseases via GSH depletion, ROS production, mitochondrial dysfunction, cell cycle disturbance and the induction of apoptosis. These events are related to the production of superoxide radicals and hydrogen peroxide.

Original languageEnglish
Pages (from-to)83-96
Number of pages14
JournalCellular and Molecular Life Sciences
Volume61
Issue number1
DOIs
Publication statusPublished - Jan 2004
Externally publishedYes

Fingerprint

Piper betle
KB Cells
Toxicity
Reactive Oxygen Species
Cell Cycle Checkpoints
Epithelial Cells
Cells
Apoptosis
Inflorescence
Fluorescence
Mastication
Cell Cycle
Mouth Diseases
Oral Submucous Fibrosis
Areca
Leukoplakia
Nuts
Rhodamines
Deferoxamine
Mitochondrial Membrane Potential

Keywords

  • Apoptosis
  • Betel quid
  • Cell cycle
  • Glutathione
  • Hydroxychavicol
  • Mitochondrial membrane potential
  • Reactive oxygen species

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Cell Biology

Cite this

Reactive oxygen species are crucial for hydroxychavicol toxicity toward KB epithelial cells. / Jeng, J. H.; Wang, Y. J.; Chang, W. H.; Wu, H. L.; Li, C. H.; Uang, B. J.; Kang, J. J.; Lee, J. J.; Hahn, L. J.; Lin, B. R.; Chang, M. C.

In: Cellular and Molecular Life Sciences, Vol. 61, No. 1, 01.2004, p. 83-96.

Research output: Contribution to journalArticle

Jeng, JH, Wang, YJ, Chang, WH, Wu, HL, Li, CH, Uang, BJ, Kang, JJ, Lee, JJ, Hahn, LJ, Lin, BR & Chang, MC 2004, 'Reactive oxygen species are crucial for hydroxychavicol toxicity toward KB epithelial cells', Cellular and Molecular Life Sciences, vol. 61, no. 1, pp. 83-96. https://doi.org/10.1007/s00018-003-3272-8
Jeng, J. H. ; Wang, Y. J. ; Chang, W. H. ; Wu, H. L. ; Li, C. H. ; Uang, B. J. ; Kang, J. J. ; Lee, J. J. ; Hahn, L. J. ; Lin, B. R. ; Chang, M. C. / Reactive oxygen species are crucial for hydroxychavicol toxicity toward KB epithelial cells. In: Cellular and Molecular Life Sciences. 2004 ; Vol. 61, No. 1. pp. 83-96.
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abstract = "Betel quid (BQ) chewing shows a strong correlation to the incidence of oral submucous fibrosis (OSF), leukoplakia and oral cancer. BQ contains mainly areca nut, lime, Piper betle leaf (PBL) and the inflorescence of P. betle (IPB). Hydroxychavicol (4-allyl-catechol, HC), as a major phenolic compound in PBL and IPB, is shown to induce oxidative stress, glutathione (GSH) depletion and cell cycle deregulation. Using bivariate BrdU/PI flow cytometry, KB cells in DNA synthesis (S phase) are shown to be sensitive to the toxic effect of HC and show cell cycle arrest and apoptosis following exposure to 0.1 and 0.3 mM HC. HC-induced apoptosis and cell cycle arrest are associated with mitochondrial membrane potential (Δψm) depolarization as revealed by a decrease in rhodamine fluorescence. N-acetyl-L-cysteine (1 mM), superoxide dismutase (100 U/ml) and catalase (1000 U/ml) were effective in prevention of HC-induced GSH depletion (as indicated by chloromethylfluorescein fluorescence), reactive oxygen species (ROS) production (by dichlorofluorescein fluorescence), cell cycle arrest and apoptosis. However, dimethylthiourea (2 mM), neocuproine (1 mM), 1,10-phenanthroline (200 μM) and desferrioxamine (0.5 mM) showed little effect on HC-induced cell changes. HC elevated the cellular and mitochondrial GSH levels at moderate concentrations (0.05-0.1 mM), whereas at a concentration of 0.3 mM, inhibitory effects were noted. These results indicate that HC consumption may be associated with BQ-chewing-related oral mucosal diseases via GSH depletion, ROS production, mitochondrial dysfunction, cell cycle disturbance and the induction of apoptosis. These events are related to the production of superoxide radicals and hydrogen peroxide.",
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AU - Li, C. H.

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AU - Kang, J. J.

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