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Eugenol triggers different pathobiological effects on human oral mucosal fibroblasts
1School of Dentistry, College of Medicine, National Taiwan University, Taipei, ROC.
Journal of Dental Research
|May 1, 1994
Summary
Eugenol, found in betel quid (BQ), shows cytotoxicity to oral fibroblasts at high concentrations, depleting glutathione (GSH) and ATP. However, lower concentrations may offer protection against oxidative stress.
Area of Science:
- Oral pathology
- Cell biology
- Toxicology
Background:
- Betel quid (BQ) chewing is prevalent in some regions and linked to oral diseases.
- Eugenol is a major component of BQ with potential biological effects.
- Understanding eugenol's impact on oral tissues is crucial for disease prevention.
Purpose of the Study:
- To investigate the pathobiological effects of eugenol on oral mucosal fibroblasts.
- To determine the concentration- and time-dependent cytotoxicity of eugenol.
- To elucidate the mechanisms underlying eugenol's effects, including its impact on glutathione (GSH), ATP, and lipid peroxidation.
Main Methods:
- Cultured human oral mucosal fibroblasts were exposed to varying concentrations of eugenol.
- Cell viability was assessed using standard assays.
- Levels of intracellular glutathione (GSH) and ATP were measured.
- Lipid peroxidation and xanthine oxidase activity were evaluated.
- DNA strand break activity was assessed.
Main Results:
- Eugenol exhibited cytotoxicity to oral fibroblasts at concentrations >3 mmol/L in a dose- and time-dependent manner.
- Cytotoxicity was linked to intracellular glutathione (GSH) depletion.
- Eugenol decreased cellular ATP levels and inhibited lipid peroxidation.
- Inhibition of lipid peroxidation was partly due to dose-dependent inhibition of xanthine oxidase (IC50 ≈ 0.3 mmol/L).
- No DNA strand breaks were observed at concentrations up to 3 mmol/L.
Conclusions:
- High concentrations of eugenol from BQ may contribute to oral submucous fibrosis and oral cancer via cytotoxicity.
- Low concentrations (<1 mmol/L) of eugenol may offer cytoprotection against reactive oxygen species-induced genetic damage by inhibiting xanthine oxidase and lipid peroxidation.