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A diet containing fish oil and pectin ameliorates radiation‐enhanced colon carcinogenesis by suppression of PPAR δ and PGE synthase‐2 (PGES 2 )and elevation of PGE 3
Author(s) -
Vanamala J.,
Glagolenko A.,
Yang P.,
Carroll R.J.,
Murphy M.E.,
Newman R.A.,
Chapkin R.S.,
Turner N.D.,
Lupton J.R.
Publication year - 2007
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.21.5.a166
Subject(s) - fish oil , fish <actinopterygii> , pectin , elevation (ballistics) , medicine , delta , biology , chemistry , endocrinology , food science , fishery , physics , astronomy
Radiation‐enhanced carcinogenesis is a major impediment to long‐duration space flight that dietary countermeasures may potentially ameliorate. We have shown that dietary fish oil/pectin (FP) may protect against colon cancer by enhancing spontaneous colonocyte apoptosis. To investigate the mechanism of action, we provided rats (n = 40) with diets containing the combination of FP or corn oil/cellulose (CC). Rats were exposed to 0 or 1 Gy, 1 GeV/nucleon Fe‐ion, 3 wk after starting the diets. All rats were injected with AOM (15 mg/kg), 10 and 17 d after irradiation. We measured the levels of colonocyte apoptosis (TUNEL), PGES 2 and PPARδ (Westerns), and PGE 2 and PGE 3 (LC/MS/MS) 31 wk after the last AOM injection. The FP induced higher (P< 0.01) apoptotic indices which are associated with suppression of the anti‐apoptotic mediators PGES 2 (P=0.045), PGE 2 (P=0.0001), and PPARδ (P=0.0085) compared to the CC diet in AOM only and AOM + radiation rats. Moreover, FP induced greater (P< 0.01) pro‐apoptotic PGE 3 in irradiated rats. These results indicate that FP counteracted the radiation elevated (P=0.045) anti‐apoptotic mediators (PPARδ and PGES 2 ) by up‐regulating (P=0.033) pro‐apoptotic PGE 3 levels. Thus, the FP diet may protect against radiation‐enhanced suppression of apoptosis during colon carcinogenesis via elevation of PGE 3 levels. Funded by AICR 05B094, NIH CA61750, NSBRI NASA NCC 9–58, CA59034 and NIEHS P30‐ES09106.