Open AccessLack of modifying effects of 4‐tert‐octylphenol and benzyl butyl phthalate on 3, 2′‐dimethyl‐4‐aminobiphenyl‐induced prostate carcinogenesis in rats
Author(s) -
Kohno Hiroyuki,
Suzuki Rikako,
Sugie Shigeyuki,
Tsuda Hiroyuki,
Tanaka Takuji
Publication year - 2004
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2004.tb03206.x
Subject(s) - proliferating cell nuclear antigen , carcinogenesis , chemistry , prostate , subcutaneous injection , medicine , endocrinology , cancer , immunohistochemistry
The modifying effects of dietary feeding of two estrogenic compounds, 4‐tert‐octylphenol (tOP) and benzyl butyl phthalate (BBP), on 3, 2′‐dimethyl‐4‐aminobiphenol (DMAB)‐induced prostatic carcinogenesis were investigated in male F344 rats. We also assessed the effects of the test compounds on the proliferating cell nuclear antigen (PCNA) index in induced neoplasms, prostatic intra‐epithelial neoplasm (PIN), and non‐lesional glands in the prostate. To induce prostatic neoplasms, rats were given subcutaneous injections of DMAB (25 mg/kg body weight) every other week, 10 times in total. They also received the experimental diet containing 10 or 100 ppm t OP and BBP for 40 weeks, starting 1 week after the last dosing of DMAB. DMAB exposure produced prostatic adenocarcinoma with an incidence of 41.2% at the end of the study (week 60). Dietary administration of tOP and BBP did not affect the incidence of prostatic adenocarcinoma: 43.8% in the DMAB→10 ppm tOP group; 25.0% in the DMAB→100 ppm t OP group; 43.8% in the DMAB→10 ppm BBP group; and 43.8% in the DMAB→100 ppm BBP group. The PCNA indices in adenocarcinomas, PIN, and non‐lesional glands in rats treated with DMAB and t OP or BBP were slightly lower than that of the DMAB alone group, but the differences were not statistically significant. These results might suggest that dietary feeding of the estrogenic compounds t OP and BBP did not modulate DMAB‐induced prostatic carcinogenesis in rats.