Effects of dietary N-(4-hydroxyphenyl)retinamide on N-nitrosomethylbenzylamine metabolism and esophageal tumorigenesis in the Fischer 344 rat

J Natl Cancer Inst. 2001 Jul 4;93(13):990-8. doi: 10.1093/jnci/93.13.990.

Abstract

Background: 9-cis-Retinoic acid (9-cis-RA) and N-(4-hydroxyphenyl)retinamide (4-HPR) are effective chemopreventive agents against epithelial tumors in the oral cavity, breast, and prostate. We tested the inhibitory activity of these retinoids against N-nitrosomethylbenzylamine (NMBA)-induced tumorigenesis in the rat esophagus.

Methods: Male Fischer 344 rats were randomly assigned to receive diets either lacking or containing 9-cis-RA or 4-HPR for 1 week before tumor initiation with NMBA and then for the duration of the study. NMBA metabolism, O(6)-methylguanine adduct formation, and cytochrome P450 messenger RNA (mRNA) expression in the esophagi of the rats were studied to investigate the mechanisms by which dietary 4-HPR affects tumorigenesis. All statistical tests were two-sided.

Results: Dietary 4-HPR resulted in a dose-dependent and statistically significant enhancement (P<.05) of tumorigenesis in response to NMBA. In two different tumor bioassays, the mean tumor multiplicity for rats fed the highest concentration of dietary 4-HPR (0.8 g/kg diet) was increased by 5.9 tumors (95% confidence interval [CI] = 1.7 to 10.1 tumors) and 6.7 tumors (95% CI = 5.6 to 7.8 tumors) compared with the mean tumor multiplicity for rats that received the control diet lacking 4-HPR. Animals fed diets containing 9-cis-RA displayed no statistically significant increase in tumorigenesis. Compared with animals fed a diet lacking 4-HPR, animals fed 4-HPR had increased NMBA metabolism in esophageal explant cultures and had higher levels of O(6)-methylguanine DNA adducts and CYP2A3 mRNA in their esophagi.

Conclusions: Dietary 4-HPR enhances tumorigenesis in response to NMBA in the rat esophagus by increasing tumor initiation events. Dietary 4-HPR may exert paradoxical effects at some sites, such as the aerodigestive tract, by modulating the bioactivation of carcinogens in target tissues.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Alitretinoin
  • Animals
  • Antineoplastic Agents / administration & dosage
  • Antineoplastic Agents / therapeutic use*
  • Carcinogens
  • Cytochrome P-450 Enzyme System / metabolism
  • DNA Adducts
  • Dimethylnitrosamine / analogs & derivatives
  • Dimethylnitrosamine / metabolism*
  • Esophageal Neoplasms / chemically induced
  • Esophageal Neoplasms / drug therapy*
  • Esophagus / drug effects
  • Fenretinide / administration & dosage
  • Fenretinide / therapeutic use*
  • Male
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Inbred F344
  • Retinoids / therapeutic use
  • Time Factors
  • Tretinoin / administration & dosage
  • Tretinoin / therapeutic use

Substances

  • Antineoplastic Agents
  • Carcinogens
  • DNA Adducts
  • RNA, Messenger
  • Retinoids
  • Fenretinide
  • Alitretinoin
  • Tretinoin
  • Cytochrome P-450 Enzyme System
  • nitrosobenzylmethylamine
  • Dimethylnitrosamine