Effect of dietary aromatic isothiocyanates fed subsequent to the administration of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone on lung tumorigenicity in mice

M. A. Morse, J. C. Reinhardt, S. G. Amin, S. S. Hecht, G. D. Stoner, F. L. Chung

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Abstract

Naturally-occurring aromatic isothiocyanates, benzyl isothiocyanate (BITC) and phenethyl isothiocyanate (PEITC), were tested for their post-treatment effects on lung tumorigenicity by the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in A J mice. Mice at 7 weeks of age were administered a single i.p. dose of NNK (10 μmol/mouse). One week after NNK dosing, mice were placed on AIN-76A diet containing 1 or 3 μmol/g diet of BITC or PEITC. The control group was maintained on AIN-76A diet after NNK administration. Mice were killed 16 week after NNK treatment and lung adenomas were counted. The results showed mice fed control diet developed 7.8 tumors/mouse. Mice fed PEITC at concentrations of 1 or 3 μmol/g diet had 8.2 or 6.1 tumors/mouse, respectively. Feeding BITC at 1 μmol/g diet resulted in a tumor yield of 8.0 tumors/mouse, whereac BITC diet at 3 μmol/g diet gave 5.2 tumors/mouse, a small but significant inhibition. However, in the high BITC dose group, a loss in weight gain due to reduced food intake was noted. The results of this study showed that post-treatment of aromatic isothiocyanates had little, if any, effect on NNK lung tumorigenicity in A J mice. This is in contrast to our previous findings in which pretreatment with PEITC greatly inhibited lung tumor induction by NNK in A J mice and suggests that tumor inhibition by PEITC is due to inhibition of NNK metabolic activation.

Original languageEnglish (US)
Pages (from-to)225-230
Number of pages6
JournalCancer Letters
Volume49
Issue number3
DOIs
StatePublished - Mar 1990

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Isothiocyanates
Lung
Diet
Neoplasms
4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone
Nitrosamines
Adenoma

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

@article{207df2d0fe1b4bc29ea7470e5f331b78,
title = "Effect of dietary aromatic isothiocyanates fed subsequent to the administration of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone on lung tumorigenicity in mice",
abstract = "Naturally-occurring aromatic isothiocyanates, benzyl isothiocyanate (BITC) and phenethyl isothiocyanate (PEITC), were tested for their post-treatment effects on lung tumorigenicity by the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in A J mice. Mice at 7 weeks of age were administered a single i.p. dose of NNK (10 μmol/mouse). One week after NNK dosing, mice were placed on AIN-76A diet containing 1 or 3 μmol/g diet of BITC or PEITC. The control group was maintained on AIN-76A diet after NNK administration. Mice were killed 16 week after NNK treatment and lung adenomas were counted. The results showed mice fed control diet developed 7.8 tumors/mouse. Mice fed PEITC at concentrations of 1 or 3 μmol/g diet had 8.2 or 6.1 tumors/mouse, respectively. Feeding BITC at 1 μmol/g diet resulted in a tumor yield of 8.0 tumors/mouse, whereac BITC diet at 3 μmol/g diet gave 5.2 tumors/mouse, a small but significant inhibition. However, in the high BITC dose group, a loss in weight gain due to reduced food intake was noted. The results of this study showed that post-treatment of aromatic isothiocyanates had little, if any, effect on NNK lung tumorigenicity in A J mice. This is in contrast to our previous findings in which pretreatment with PEITC greatly inhibited lung tumor induction by NNK in A J mice and suggests that tumor inhibition by PEITC is due to inhibition of NNK metabolic activation.",
author = "Morse, {M. A.} and Reinhardt, {J. C.} and Amin, {S. G.} and Hecht, {S. S.} and Stoner, {G. D.} and Chung, {F. L.}",
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Effect of dietary aromatic isothiocyanates fed subsequent to the administration of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone on lung tumorigenicity in mice. / Morse, M. A.; Reinhardt, J. C.; Amin, S. G.; Hecht, S. S.; Stoner, G. D.; Chung, F. L.

In: Cancer Letters, Vol. 49, No. 3, 03.1990, p. 225-230.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Effect of dietary aromatic isothiocyanates fed subsequent to the administration of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone on lung tumorigenicity in mice

AU - Morse, M. A.

AU - Reinhardt, J. C.

AU - Amin, S. G.

AU - Hecht, S. S.

AU - Stoner, G. D.

AU - Chung, F. L.

PY - 1990/3

Y1 - 1990/3

N2 - Naturally-occurring aromatic isothiocyanates, benzyl isothiocyanate (BITC) and phenethyl isothiocyanate (PEITC), were tested for their post-treatment effects on lung tumorigenicity by the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in A J mice. Mice at 7 weeks of age were administered a single i.p. dose of NNK (10 μmol/mouse). One week after NNK dosing, mice were placed on AIN-76A diet containing 1 or 3 μmol/g diet of BITC or PEITC. The control group was maintained on AIN-76A diet after NNK administration. Mice were killed 16 week after NNK treatment and lung adenomas were counted. The results showed mice fed control diet developed 7.8 tumors/mouse. Mice fed PEITC at concentrations of 1 or 3 μmol/g diet had 8.2 or 6.1 tumors/mouse, respectively. Feeding BITC at 1 μmol/g diet resulted in a tumor yield of 8.0 tumors/mouse, whereac BITC diet at 3 μmol/g diet gave 5.2 tumors/mouse, a small but significant inhibition. However, in the high BITC dose group, a loss in weight gain due to reduced food intake was noted. The results of this study showed that post-treatment of aromatic isothiocyanates had little, if any, effect on NNK lung tumorigenicity in A J mice. This is in contrast to our previous findings in which pretreatment with PEITC greatly inhibited lung tumor induction by NNK in A J mice and suggests that tumor inhibition by PEITC is due to inhibition of NNK metabolic activation.

AB - Naturally-occurring aromatic isothiocyanates, benzyl isothiocyanate (BITC) and phenethyl isothiocyanate (PEITC), were tested for their post-treatment effects on lung tumorigenicity by the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in A J mice. Mice at 7 weeks of age were administered a single i.p. dose of NNK (10 μmol/mouse). One week after NNK dosing, mice were placed on AIN-76A diet containing 1 or 3 μmol/g diet of BITC or PEITC. The control group was maintained on AIN-76A diet after NNK administration. Mice were killed 16 week after NNK treatment and lung adenomas were counted. The results showed mice fed control diet developed 7.8 tumors/mouse. Mice fed PEITC at concentrations of 1 or 3 μmol/g diet had 8.2 or 6.1 tumors/mouse, respectively. Feeding BITC at 1 μmol/g diet resulted in a tumor yield of 8.0 tumors/mouse, whereac BITC diet at 3 μmol/g diet gave 5.2 tumors/mouse, a small but significant inhibition. However, in the high BITC dose group, a loss in weight gain due to reduced food intake was noted. The results of this study showed that post-treatment of aromatic isothiocyanates had little, if any, effect on NNK lung tumorigenicity in A J mice. This is in contrast to our previous findings in which pretreatment with PEITC greatly inhibited lung tumor induction by NNK in A J mice and suggests that tumor inhibition by PEITC is due to inhibition of NNK metabolic activation.

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