URINARY-EXCRETION OF 3-METHYLADENINE AFTER CONSUMPTION OF FISH CONTAINING HIGH-LEVELS OF DIMETHYLAMINE

Citation
Lb. Fay et al., URINARY-EXCRETION OF 3-METHYLADENINE AFTER CONSUMPTION OF FISH CONTAINING HIGH-LEVELS OF DIMETHYLAMINE, Carcinogenesis, 18(5), 1997, pp. 1039-1044
Citations number
48
Categorie Soggetti
Oncology
Journal title
ISSN journal
01433334
Volume
18
Issue
5
Year of publication
1997
Pages
1039 - 1044
Database
ISI
SICI code
0143-3334(1997)18:5<1039:UO3ACO>2.0.ZU;2-R
Abstract
The urinary excretion of the DNA alkylation product, 3-methyladenine ( 3-MeAde), was measured in human volunteers who were on controlled diet s and consumed fresh fish, or frozen-stored fish that contained 50-fol d higher levels of dimethylamine (DMA), with or without ingested nitra te. DMA potentially could react with nitrosating agents in the diet or within the body, and produce the potent carcinogen N-nitrosodimethyla mine (NDMA), which can then react with DNA to form several adducts inc luding 3-MeAde. Our findings show that there was no increase in urinar y levels of 3-MeAde after consumption of fish preserved by frozen stor age relative to levels after consumption of fresh fish. Furthermore, c onsumption of 225 mg sodium nitrate (equal to the nitrate content in a large glass of beet juice) at 1 h prior to consumption of the frozen- stored fish did not increase urinary 3-MeAde levels as would be expect ed if nitrate enhanced endogenous nitrosation of DMA. In contrast, uri nary excretion of 3-MeAde from a volunteer who was a moderate cigarett e smoker (11 cigarettes per day) was approximate to 3- to 8-fold highe r than dietary 3-MeAde intake. These findings indicate that consumptio n of high levels of DMA in fish does not result in detectable levels o f NDMA formation and genetic damage as measured by the urinary biomark er 3-MeAde.