Lack of promotion of N-butyl-N-(4-hydroxybutyl)nitrosamine-initiated urinary bladder carcinogenesis in mice by rat cancer promoters.
The effects of dietary exposure to sodium L-ascorbate (Na-AsA), butylated hydroxyanisole (BHA), and diphenyl on the development of urinary bladder tumors in a mouse two-stage carcinogenesis model were examined. Male B6C3F1 mice received 0.05% N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) in the drinking water for 4 weeks and were then treated with 5% Na-AsA, 1% BHA, or 1% diphenyl for 32 weeks. None of these chemicals enhanced the development of either preneoplastic or neoplastic lesions in the urinary bladder. Furthermore, DNA synthesis levels of urinary bladder epithelium in mice treated with each substance alone for 8 weeks were not elevated significantly, although Na-AsA was associated with a significant increase in the urinary pH value and Na+ concentration. The results indicate that Na-AsA, BHA, and diphenyl do not exert an enhancing influence on mouse bladder carcinogenesis, in clear contrast to the case in the rat.
Tamano
S
S
First Department of Pathology, Nagoya City University Medical School, Japan.
Asakawa
E
E
Boomyaphiphat
P
P
Masui
T
T
Fukushima
S
S
D000818:Animals; D001205:Ascorbic Acid / Q000633:toxicity; D001713:Biphenyl Compounds / Q000633:toxicity; D002083:Butylated Hydroxyanisole / Q000633:toxicity; D002085:Butylhydroxybutylnitrosamine / Q000633:toxicity*; D002273:Carcinogens / Q000633:toxicity*; D008297:Male; D051379:Mice; D051381:Rats; D001749:Urinary Bladder Neoplasms / Q000139:chemically induced*
D001205:Ascorbic Acid; D001713:Biphenyl Compounds; D002083:Butylated Hydroxyanisole; D002085:Butylhydroxybutylnitrosamine; D002273:Carcinogens; C010574:biphenyl