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Inhibition effect of Vitamine E δ‐tocotrienol on PhIP/DSS‐induced colon carcinogenesis in CYP1A‐humanized mice (LB325)
Author(s) -
Chen YuKuo,
Liu Anna,
Lee MaoJung,
Wang Hong,
Cheung Connie,
Yang Chung S.
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb325
Subject(s) - tocotrienol , azoxymethane , carcinogenesis , colorectal cancer , chemistry , pharmacology , colon carcinoma , anticarcinogen , heterocyclic amine , carcinogen , cancer research , medicine , biochemistry , cancer , vitamin e , antioxidant , tocopherol , gene
Our previous research indicated that combination of 2‐amino‐1‐methyl‐6‐phenylimidazo[4,5‐b]pyridine (PhIP), the most abundant heterocyclic amine produced during the cooking of meats and fish, with dextran sodium sulfate (DSS) rapidly induced colon carcinogenesis in transgenic CYP1A‐humanized mice (hCYP1A‐mice). Herein, we modulated the dosage of DSS (0.8‐1.5%) to establish a suitable model for cancer prevention research and to evaluate the inhibition effect of δ‐tocotrienol (δ‐T3) on colon carcinogenesis. The treatment with 200 mg/kg PhIP, followed by 1% DSS in the drinking water for 7 days moderately induced colon carcinogenesis in hCYP1A‐mice with a tumor multiplicity of 4.17 ± 0.58 at week 8. Tumor multiplicity was reduced in 0.025% and 0.5% δ‐T3 treatment groups by 49% (P < 0.05) and 58% (P < 0.01), respectively. Supplementation with δ‐T3 also increased the respective levels of tocotrienol in the serum and colon tissues. These results demonstrate the inhibitory effect of δ‐T3 against colon carcinogenesis, and the inhibitory activity may be due mainly to the actions of δ‐T3. Grant Funding Source : NSC‐102‐2221‐E‐020‐021

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