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

G.K. Pot, N. Habermann, G. Majsak-Newman, L.J. Harvey, A. Geelen, B.J.M. Witteman, P.C. van de Meeberg, A.R. Hart, G. Schaafsma, G.J.E.J. Hooiveld, M. Glei, E.K. Lund, B.L. Pool-Zobel, E. Kampman

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11 Citations (Scopus)


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.
Original languageEnglish
Pages (from-to)1087-1091
Issue number6
Publication statusPublished - 2010


  • polyunsaturated fatty-acids
  • rectal cell-proliferation
  • fecal water genotoxicity
  • colorectal-cancer risk
  • induced dna-damage
  • comet assay
  • oxidative stress
  • eicosapentaenoic acid
  • dietary
  • carcinogenesis


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