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Inhibition of nitric oxide-induced apoptosis by nicotine in oral epithelial cells

Abhijit G Banerjee1, Velliyur K Gopalakrishnan, Jamboor K Vishwanatha

  • 1Department of Oral Biology, Dental Diagnostic and Surgical Sciences, University of Manitoba, Health Science Center Campus, Winnipeg, MB, Canada, R3E0W2. banerjea@cc.umanitoba.ca

Molecular and Cellular Biochemistry
|July 20, 2007
PubMed

Insights

Smokeless tobacco use contributes to oral cancer by inhibiting apoptosis, programmed cell death, through nicotine

Area of Science:

  • Oncology
  • Molecular Biology
  • Toxicology

Background:

  • Smokeless tobacco use is a significant risk factor for oral cancer.
  • The precise molecular mechanisms driving smokeless tobacco-induced oral carcinogenesis remain unclear.
  • Understanding apoptosis regulation in oral epithelial cells is crucial for cancer prevention strategies.

Purpose of the Study:

  • To investigate the impact of smokeless tobacco exposure on oral epithelial cell apoptosis.
  • To elucidate the role of nicotine and nitric oxide (NO) in smokeless tobacco-induced apoptosis.
  • To explore the potential link between nicotine's anti-apoptotic effects and oral cancer development.

Main Methods:

  • Exposure of oral epithelial cells to smokeless tobacco extract (STE) and varying nicotine concentrations.
  • Assessment of apoptosis using cell viability assays and detection of apoptotic markers.
  • Measurement of nitric oxide (NO) production and radical scavenging activity.
  • Analysis of nitrotyrosine accumulation in transformed cells using 3-NT ELISA.

Main Results:

  • STE induced apoptosis in oral epithelial cells in a dose-dependent manner.
  • Nicotine inhibited STE-induced apoptosis at concentrations of 1 mM and above.
  • Nicotine's anti-apoptotic effect was linked to the down-regulation of nitric oxide (NO) production.
  • Nicotine acted as a sink for NO radicals, leading to increased nitrotyrosine in transformed cells.

Conclusions:

  • Nicotine's inhibition of NO-induced apoptosis may contribute to smokeless tobacco-associated oral carcinogenesis.
  • The anti-apoptotic action of nicotine highlights a critical mechanism in tobacco-induced cancer.
  • Findings suggest the need for targeted strategies in tobacco cessation programs to address nicotine's role in cancer progression.

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