Effect of dietary meat and fish on endogenous nitrosation, inflammation and genotoxicity of faecal water.

TitleEffect of dietary meat and fish on endogenous nitrosation, inflammation and genotoxicity of faecal water.
Publication TypeJournal Article
Year of Publication2010
AuthorsJoosen, AMCP, Lecommandeur, E, Kuhnle, GGC, Aspinall, SM, Kap, L, Rodwell, SA
JournalMutagenesis
Volume25
Issue3
Pagination243-7
Date Published2010 May
ISSN1464-3804
KeywordsAdult, Aged, Aged, 80 and over, Animals, Biological Markers, Diet, DNA Breaks, Feces, Feeding Behavior, Female, Fishes, Heme, Humans, Inflammation, Male, Meat, Middle Aged, Mutagens, Nitrosation, Nitroso Compounds, Water, Young Adult
Abstract

N-3 polyunsaturated fatty acids have been associated with reduced colon tumorigenesis. However, their association with colorectal cancer incidence is not conclusive. We investigated the influence of isocaloric replacement of red meat with fatty fish on endogenous nitrosation, inflammation and genotoxicity of faecal water in apparently healthy human volunteers on controlled diets. Fourteen volunteers consumed a high red meat, a combined red meat/fish and a high fish diet for 8 days each. Faecal homogenates were analysed for haem, nitroso compounds (NOC) and calprotectin and associated supernatants for genotoxicity. Both faecal NOC and haem excretion decreased with more fish and less meat in the diet. Nitrosyl iron (FeNO) was the main contributor to total NOC on all diets. The proportion of other NOC increased with more fish and less meat in the diet (P = 0.01), resulting in a non-statistically significant decrease in the proportion of FeNO on the fish diet. There was no statistically significant difference in faecal calprotectin (P = 0.54) and faecal water-induced DNA strand breaks and oxidized purines and pyrimidines between the diets (P > 0.36). Increasing fish intake and reducing the intake of red meat does not seem to have an effect on inflammation and faecal water-induced (oxidative) DNA damage; however, it does reduce the formation of mutagenic and potentially carcinogenic NOC and may as such beneficially affect colorectal risk.

DOI10.1093/mutage/gep070
Alternate JournalMutagenesis
Citation Key10.1093/mutage/gep070
PubMed ID20106932
Grant ListMC_U105630924 / / Medical Research Council / United Kingdom
/ / Medical Research Council / United Kingdom