Increasing fish consumption does not affect genotoxicity markers in the colon in an intervention study

TY - JOUR

T1 - Increasing fish consumption does not affect genotoxicity markers in the colon in an intervention study

AU - Pot, Gerda K

AU - Habermann, Nina

AU - Majsak-Newman, Gosia

AU - Harvey, Linda J

AU - Geelen, Anouk

AU - Przybylska-Philips, Kasia

AU - Nagengast, Fokko M

AU - Witteman, Ben J M

AU - van de Meeberg, Paul C

AU - Hart, Andrew R

AU - Schaafsma, Gertjan

AU - Hooiveld, Guido

AU - Glei, Michael

AU - Lund, Elizabeth K

AU - Pool-Zobel, Beatrice L

AU - Kampman, Ellen

PY - 2010/6

Y1 - 2010/6

N2 - Observational studies suggest that fish consumption is associated with a decreased colorectal cancer (CRC) risk. A possible mechanism by which fish could reduce CRC risk is by decreasing colonic genotoxicity. However, concerns have also been raised over the levels of toxic compounds found in mainly oil-rich fish, which could increase genotoxicity. Therefore, the objective was to investigate the effects of fish on genotoxicity markers in the colon in a randomized controlled parallel intervention study. For a period of 6 months, subjects were randomly allocated to receive two extra weekly portions of (i) oil-rich fish (salmon), (ii) lean fish (cod) or (iii) just dietary advice (DA). The Comet Assay was used to measure the DNA damage-inducing potential of fecal water (n = 89) and DNA damage in colonocytes (n = 70) collected pre- and post-intervention as markers of genotoxicity. Genotoxicity of fecal water was not markedly changed after fish consumption: 1.0% increase in tail intensity (TI) [95% confidence interval (CI) -5.1; 7.0] in the salmon group and 0.4% increase in TI (95% CI -5.3; 6.1) in the cod group compared with the DA group. DNA damage in colonocytes was also not significantly changed after fish consumption, in either the salmon group (-0.5% TI, 95% CI -6.9; 6.0) or cod group (-3.3% TI, 95% CI -10.8; 4.3) compared with the DA group. Measurements of genotoxicity of fecal water and DNA damage in colonocytes did not correlate (r = 0.06, n = 34). In conclusion, increasing consumption of either oil-rich or lean fish did not affect genotoxicity markers in the colon.

AB - Observational studies suggest that fish consumption is associated with a decreased colorectal cancer (CRC) risk. A possible mechanism by which fish could reduce CRC risk is by decreasing colonic genotoxicity. However, concerns have also been raised over the levels of toxic compounds found in mainly oil-rich fish, which could increase genotoxicity. Therefore, the objective was to investigate the effects of fish on genotoxicity markers in the colon in a randomized controlled parallel intervention study. For a period of 6 months, subjects were randomly allocated to receive two extra weekly portions of (i) oil-rich fish (salmon), (ii) lean fish (cod) or (iii) just dietary advice (DA). The Comet Assay was used to measure the DNA damage-inducing potential of fecal water (n = 89) and DNA damage in colonocytes (n = 70) collected pre- and post-intervention as markers of genotoxicity. Genotoxicity of fecal water was not markedly changed after fish consumption: 1.0% increase in tail intensity (TI) [95% confidence interval (CI) -5.1; 7.0] in the salmon group and 0.4% increase in TI (95% CI -5.3; 6.1) in the cod group compared with the DA group. DNA damage in colonocytes was also not significantly changed after fish consumption, in either the salmon group (-0.5% TI, 95% CI -6.9; 6.0) or cod group (-3.3% TI, 95% CI -10.8; 4.3) compared with the DA group. Measurements of genotoxicity of fecal water and DNA damage in colonocytes did not correlate (r = 0.06, n = 34). In conclusion, increasing consumption of either oil-rich or lean fish did not affect genotoxicity markers in the colon.

KW - Mutagens

KW - Comet Assay

KW - Animals

KW - Colon

KW - DNA Damage

KW - Fishes

KW - Seafood

KW - Diet

KW - Colorectal Neoplasms

KW - Biological Markers

U2 - 10.1093/carcin/bgp255

DO - 10.1093/carcin/bgp255

M3 - Article

C2 - 19861650

VL - 31

SP - 1087

EP - 1091

JO - Carcinogenesis

JF - Carcinogenesis

IS - 6

ER -