Abstract |
The metabolic fate of N,N-dibutylnitrosamine (DBN) was studied in the rat, to elucidate the possibility of a correlation between its metabolism and its organotropic carcinogenicity to the urinary bladder and other organs. It was extensively metabolized in the rat, no unchanged DBN being found in the urine. DNA underwent metabolic transformation in at least three ways. The major pathways demonstrated on the basis of urinary metabolites were omega- and (omega-1)-oxidations of one butyl chain to give N-butyl-N-(3-carboxypropyl)nitrosamine ( BCPN) and N-butyl-N-(3-hydroxybutyl)nitrosamine, respectively. The third minor pathway was (omega-2)-oxidation of the butyl chain to afford N-butyl-N-(2-hydroxybutyl)nitrosamine. Both hydroxylated metabolites were excreted into the urine as such and as their glucuronic acid conjugates. The omega-oxidation of DBN to BCPN is responsible for the induction of bladder tumors in rats, while the products of the (omega-1)- or (omega-2)-oxidation may be involved in tumor induction in the liver.
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Authors | E Suzuki, M Okada |
Journal | Gan
(Gan)
Vol. 71
Issue 6
Pg. 863-70
(Dec 1980)
ISSN: 0016-450X [Print] Japan |
PMID | 7274631
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Carcinogens
- Nitrosamines
- dibutylnitrosamine
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Topics |
- Animals
- Biotransformation
- Carcinogens
(metabolism)
- Chromatography, Thin Layer
- Liver Neoplasms
(chemically induced)
- Liver Neoplasms, Experimental
(chemically induced)
- Male
- Neoplasms, Experimental
(chemically induced)
- Nitrosamines
(metabolism)
- Rats
- Urinary Bladder Neoplasms
(chemically induced)
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