Inhibition of experimental tobacco carcinogen induced head and neck carcinogenesis

Joel Schwartz, Vikki Baker, Eric Larios, Dhimant Desai, Shantu Amin

Research output: Contribution to journalArticle

12 Scopus citations

Abstract

Oral cancer models have attempted to demonstrate inhibition of oral carcinogenesis. These models used synthetic carcinogens, lacked a specific mechanism of activity or used non-physiologic doses for carcinogen or inhibitor. To correct these problems the tobacco and environmental carcinogen, dibenzo[a,l]pyrene (DB[a,l]P) (0.25%, 0.010 μM/application) was painted on the tongue and/or vitamin E acid succinate (VEas) (0.43 I.U./0.136 (μM/treatment) administered by gavages to Syrian hamsters (14 animals per group) using physiologic low doses, 5X/week. Oral cytology supplied keratinocytes after 1, 10, or 25 weeks of treatment. Cells were analyzed by flow cytometry/laser scanning cytometry. Initiation (1-6 weeks) was suppressed by reducing DNA damage (oxidation lesions: 8-oxo-dG), and repair (comet, fpg, OGG1, NTH1). Reduction in promotion (6-10 weeks) was identified by depressed proliferation (cell cycle, bromodeoxyuridine incorporation (BrdU)) and aneuploidy (propidium iodide stain). p53 and apoptosis expressions were increased (Sub G1, mitochondrion activation: Apo 2.7, and nucleosomal formation: mebstain (TUNEL)). VEas administration reduced dysplasia (10 weeks) and oral cancer formation at 25 (0/7 vs. 5/7 DB[a,l]P) and 30 weeks (3/7 vs. 6/7 DB[a,l]P). Inhibition of oral carcinogenesis by VEas involved reversal of several cellular events that contribute towards oral cancer.

Original languageEnglish (US)
Pages (from-to)611-623
Number of pages13
JournalOral Oncology
Volume40
Issue number6
DOIs
StatePublished - Jul 1 2004

All Science Journal Classification (ASJC) codes

  • Oral Surgery
  • Oncology
  • Cancer Research

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