Lack of Enhancing Effect of Lauric Acid on the Development of Aberrant Crypt Foci in Male ICR Mice Treated with Azoxymethane and Dextran Sodium Sulfate

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  • Miyamoto Shingo
    Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University
  • Suzuki Rikako
    Department of Oncologic Pathology, Kanazawa Medical University
  • Yasui Yumiko
    Department of Oncologic Pathology, Kanazawa Medical University
  • Kohno Hiroyuki
    Department of Oncologic Pathology, Kanazawa Medical University
  • Sugie Shigeyuki
    Department of Oncologic Pathology, Kanazawa Medical University
  • Murakami Akira
    Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University
  • Ohigashi Hajime
    Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University
  • Tanaka Takuji
    Department of Oncologic Pathology, Kanazawa Medical University

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The effect of lauric acid (LA), which is reported to induce cyclooxygenase (COX)-2 expression in macrophage cells (RAW 264.7) on the development of aberrant crypt foci (ACF), putative precursor lesions of colonic adenocarcinoma, was investigated in an inflammation-related mouse colon carcinogenesis model treated with azoxymethane (AOM) and dextran sulfate sodium (DSS). To induce ACF, male ICR mice were given a single intraperitoneal injection of AOM (10 mg/kg body weight) and then followed by 1% DSS in drinking water for one week, starting one week after dosing of AOM (AOM/DSS group). The AOM/DSS/LA group was fed with a diet containing 1% LA for 7 weeks, starting one week after the cessation of DSS administration. Other groups included the AOM/LA group given AOM and 1% LA diet for 9 weeks, the DSS/LA group given DSS and the diet with 1% LA, the AOM group that received AOM alone, the DSS group given DSS alone in drinking water, the LA group fed with 1% LA-containing diet alone, and the untreated group. At week 10 (end of the study), the frequency of ACF did not significantly differ between the AOM/DSS group (7.4 ± 3.0) and the AOM/DSS/LA group (8.4 ± 5.0). The value was extremely low in the AOM/LA group (1.0 ± 1.0) and in the AOM alone group (2.4 ± 2.7). No ACF developed in other groups. Our findings suggest that dietary LA did not influence the occurrence of ACF in the AOM/DSS-induced mouse colon tumorigenesis, indicating a lack of LA enhancing effects on the early phase of inflammation-related mouse colon carcinogenesis.

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