Open AccessCo‐carcinogenic Effect of Retinyl Acetate on Forestomach Carcinogenesis of Male F344 Rats Induced with Butylated Hydroxyanisole
Author(s) -
Hasegawa Ryohei,
Takahashi Michihito,
Furukawa Fumio,
Toyoda Kazuhiro,
Sato Hidetaka,
Hayashi Yuzo
Publication year - 1988
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1988.tb01594.x
Subject(s) - butylated hydroxyanisole , carcinogen , carcinogenesis , hyperplasia , endocrinology , medicine , papilloma , retinyl acetate , chemistry , anticarcinogen , nitrosamine , proventriculus , biology , pathology , antioxidant , retinol , biochemistry , anatomy , cancer , vitamin
The potential modifying effect of retinyl acetate (RA) on butylated hydroxyanisole (BHA)‐induced rat forestomach tumorigenesis was examined. Male F344 rats, 5 weeks of age, were maintained on diet containing 1% or 2% BHA by weight and simultaneously on drinking water supplemented with RA at various concentrations (w/v) for 52 weeks. In groups given 2% BHA, although marked hyperplastic changes of the forestomach epithelium were observed in all animals, co‐administration of 0.25% RA significantly (P<0.05) increased the incidence of forestomach tumors (squamous cell papilloma and carcinoma) to 60% (9/15, 2 rats with carcinoma) from 15% (3/20, one rat with carcinoma) in the group given RA‐free water. In rats given 1% BHA, RA co‐administered at a dose of 0.05, 0.1, 0.2 or 0.25% showed a dose‐dependent enhancing effect on the development of the BHA‐induced epithelial hyperplasia. Tumors, all papillomas, were induced in 3 rats (17%) with 0.25% RA and in one rat (10%) with 0.05% RA co‐administration. RA alone did not induce hyperplastic changes in the forestomach. These findings indicate that RA acted as a co‐carcinogen in the BHA forestomach carcinogenesis of the rat.