It is known that some
nitrosamines preferably affect particular organs because of their organospecificity.
Diethylnitrosamine (DEN) is one of the most powerful
nitrosamines for experimentally inducing
esophagus cancer. The present study aimed to evaluate the rate and type of epithelial lesions induced by DEN in mice. We also assessed the role of alcohol and
N-nitrosonornicotine (NNN) as promoters of this
carcinogenesis. A total of 208 female mice (Mus musculus) were allocated to five experimental groups: group 1, water only (controls); group 2, DEN + water; group 3, DEN + NNN; group 4, DEN + 6% alcohol
solution; group 5, DEN + NNN + 6% alcohol
solution. Animals in groups 2, 3, 4 and 5 received DEN (0.04 ml/l) three times per week, and during the following 4 days they received the other solutions. NNN was provided at a final concentration of 30 mg/l. The overall experimental period was 180 days. At the end of this time, the animals were killed and their esophagus was dissected for macro- and microscopic analysis. There was no significant difference in relation to the size of the esophagus and to the average DEN intake by the animals (p > 0.05). A statistically significant difference (p < 0.0001) was observed between controls and all other experimental groups. There was no significant difference among experimental groups treated with
carcinogens (p > 0.05). The average incidence of
cancer was 85.4%. The experimental model used in the present study is a very potent
indicator of
esophagus cancer. Owing to the high incidence for
cancer observed in the present study, it was not possible to assess the effect of alcohol and NNN as inducers for the development of
esophageal cancer.