Effect of Increased Water Intake on Urinary DNA Adduct Levels and Mutagenicity in Smokers: A Randomized Study.

Inmaculada Buendia Jimenez,Pascaline Picard,Michel De Meo,Pascaline Richardot,Glenn Talaska,Eve M Lepicard

doi:10.1155/2015/478150

Inmaculada Buendia Jimenez, Pascaline Picard + Show 4 more

Open Access

https://doi.org/10.1155/2015/478150

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Journal: Disease markers	Publication Date: Jan 1, 2015
Citations: 7	License type: CC BY 3.0

Affiliation: Danone (France), University of Cincinnati

Abstract

The association between fluid intake and bladder cancer risk remains controversial. Very little is known about to which extent the amount of water intake influences the action of excreting toxics upon the urinary system. This proof of concept trial investigates the effect of water intake on mutagenesis in smokers, a high risk population for bladder cancer. Methods. Monocentric randomized controlled trial. Inclusion Criteria. Male subjects aged 2045–45 y/o, smokers, and small drinkers (24-hour urinary volume <1 L and osmolality >700 mOsmol/kg). Outcomes. 4-ABP DNA adducts formation in exfoliated bladder cells in 24-hour urine collection and urinary mutagenicity in 24-hour urine. Test Group. Subjects consumed 1.5 L daily of the study product (EVIAN) on top of their usual water intake for 50 days. Control Group. Subjects continued their usual lifestyle habits. Results. 65 subjects were randomized. Mean age was 30 y/o and mean cigarettes per day were 20. A slight decrease in adducts formation was observed between baseline and last visit but no statistically significant difference was demonstrated between the groups. Urinary mutagenicity significantly decreased. The study shows that increasing water intake decreases urinary mutagenicity. It is not confirmed by urinary adducts formation. Further research would be necessary.

Highlights

Tobacco smoking and occupational exposure to chemicals are leading causes of urinary bladder cancer [1]
Metabolites of aromatic amines are mainly excreted in the urine [2,3,4], and bladder biopsies and exfoliated urothelial cells from exposed populations contain increased levels of DNA adducts associated with bladder cancer, benzidine and 4aminobiphenyl (4-ABP) [5, 6]
Since smokers and workers exposed to polycyclic aromatic hydrocarbons (PAH) excrete increased amounts of mutagens into their urine, it is possible that PAH contribute to the increased risk of urinary bladder cancer

Summary

Introduction

Tobacco smoking and occupational exposure to chemicals are leading causes of urinary bladder cancer [1]. This is thought to be largely due to exposure to aromatic amines, which, when activated, can react with DNA to form DNA adducts that may induce mutations in key cancer-related genes [1]. Metabolites of aromatic amines are mainly excreted in the urine [2,3,4], and bladder biopsies and exfoliated urothelial cells from exposed populations contain increased levels of DNA adducts associated with bladder cancer, benzidine and 4aminobiphenyl (4-ABP) [5, 6]. Since smokers and workers exposed to polycyclic aromatic hydrocarbons (PAH) excrete increased amounts of mutagens into their urine, it is possible that PAH contribute to the increased risk of urinary bladder cancer. In either case one Disease Markers might expect that an increase in water intake would induce lower levels of urinary mutagens, DNA adducts in the urinary bladder, and, perhaps, the risk of urinary bladder cancer

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