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Modulation of apoptosis by cancer chemopreventive agents

Francesco D'Agostini1, Alberto Izzotti, Roumen M Balansky

  • 1Department of Health Sciences, University of Genoa, via A. Pastore 1, I-16132 Genoa, Italy. fda@unige.it

Mutation Research
|September 3, 2005
PubMed

Insights

N-acetylcysteine (NAC) inhibited apoptosis in rodents exposed to cigarette smoke, counteracting gene and protein changes. Many cancer chemopreventive agents induce apoptosis, potentially indicating toxicity at high doses.

Area of Science:

  • Cell Biology
  • Toxicology
  • Cancer Chemoprevention

Background:

  • A review of 2000 studies revealed most cancer chemopreventive agents induce apoptosis.
  • Inhibition of apoptosis was consistently reported only for ascorbic acid, alpha-tocopherol, and N-acetylcysteine (NAC).
  • The role of apoptosis modulation by chemopreventive agents in response to environmental exposures requires further investigation.

Purpose of the Study:

  • To investigate the effects of specific chemopreventive agents on apoptosis in rodents exposed to cigarette smoke (CS) and UV light.
  • To determine if N-acetylcysteine (NAC) can inhibit CS-induced apoptosis and related molecular changes.
  • To explore the implications of apoptosis induction versus inhibition by chemopreventive agents in carcinogenesis and disease.

Main Methods:

  • Experimental studies in rodents exposed to mainstream (MCS) or environmental (ECS) cigarette smoke and UV-A/B light.
  • Assessment of apoptosis modulation by agents including sulindac, 5,6-benzoflavone, indole-3-carbinol, 1,2-dithiole-3-thione, oltipraz, phenethyl isothiocyanate, and NAC.
  • Analysis of gene and protein expression related to apoptosis in lung and fetal liver tissues.

Main Results:

  • Most tested chemopreventive agents did not inhibit apoptosis in response to CS or UV exposure.
  • Phenethyl isothiocyanate enhanced apoptosis in lung cells and upregulated proapoptotic genes.
  • NAC inhibited apoptosis in the respiratory tract of CS-exposed rats, attenuated gene overexpression, and normalized protein levels.
  • Transplacental administration of NAC reduced gene overexpression in the liver of fetuses exposed to ECS.

Conclusions:

  • NAC effectively inhibits cigarette smoke-induced apoptosis and related molecular alterations in rodents.
  • The frequent induction of apoptosis by many chemopreventive agents may suggest toxicity at high doses.
  • Inhibition of apoptosis by chemopreventive agents may counteract cellular stress signals, but enhancement can be detrimental in other disease contexts.

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