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Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats
by
YASUI Yumiko
, MIYASHITA Kazuo
, KOHNO Hiroyuki
, HOSOKAWA Masashi
, TANAKA Takuji
, SUZUKI Rikako
in
Adenocarcinoma
/ Animals
/ Anticarcinogenic Agents - administration & dosage
/ Azoxymethane
/ Biological and medical sciences
/ Body weight
/ Carcinogenesis
/ Colon
/ Colonic Neoplasms - chemically induced
/ Colonic Neoplasms - prevention & control
/ Diet
/ Dose-response relationship
/ Linoleic acid
/ Linolenic acid
/ Linolenic Acids - administration & dosage
/ Liver
/ Lythraceae - chemistry
/ Male
/ Medical sciences
/ Mucosa
/ Oilseeds
/ Peroxisome proliferator-activated receptors
/ Plant Oils - administration & dosage
/ Rats
/ Rats, Inbred F344
/ Receptors, Cytoplasmic and Nuclear - analysis
/ Seeds
/ Seeds - chemistry
/ Transcription Factors - analysis
/ Tumors
2004
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Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats
by
YASUI Yumiko
, MIYASHITA Kazuo
, KOHNO Hiroyuki
, HOSOKAWA Masashi
, TANAKA Takuji
, SUZUKI Rikako
in
Adenocarcinoma
/ Animals
/ Anticarcinogenic Agents - administration & dosage
/ Azoxymethane
/ Biological and medical sciences
/ Body weight
/ Carcinogenesis
/ Colon
/ Colonic Neoplasms - chemically induced
/ Colonic Neoplasms - prevention & control
/ Diet
/ Dose-response relationship
/ Linoleic acid
/ Linolenic acid
/ Linolenic Acids - administration & dosage
/ Liver
/ Lythraceae - chemistry
/ Male
/ Medical sciences
/ Mucosa
/ Oilseeds
/ Peroxisome proliferator-activated receptors
/ Plant Oils - administration & dosage
/ Rats
/ Rats, Inbred F344
/ Receptors, Cytoplasmic and Nuclear - analysis
/ Seeds
/ Seeds - chemistry
/ Transcription Factors - analysis
/ Tumors
2004
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Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats
by
YASUI Yumiko
, MIYASHITA Kazuo
, KOHNO Hiroyuki
, HOSOKAWA Masashi
, TANAKA Takuji
, SUZUKI Rikako
in
Adenocarcinoma
/ Animals
/ Anticarcinogenic Agents - administration & dosage
/ Azoxymethane
/ Biological and medical sciences
/ Body weight
/ Carcinogenesis
/ Colon
/ Colonic Neoplasms - chemically induced
/ Colonic Neoplasms - prevention & control
/ Diet
/ Dose-response relationship
/ Linoleic acid
/ Linolenic acid
/ Linolenic Acids - administration & dosage
/ Liver
/ Lythraceae - chemistry
/ Male
/ Medical sciences
/ Mucosa
/ Oilseeds
/ Peroxisome proliferator-activated receptors
/ Plant Oils - administration & dosage
/ Rats
/ Rats, Inbred F344
/ Receptors, Cytoplasmic and Nuclear - analysis
/ Seeds
/ Seeds - chemistry
/ Transcription Factors - analysis
/ Tumors
2004
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Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats
Journal Article
Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats
2004
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Overview
Pomegranate (Punica granatum L.) seed oil (PGO) contains more than 70% cis(c)9,frans(f)11,c13–18:3 as conjugated linolenic acids (CLN). Our previous short‐term experiment demonstrated that seed oil from bitter melon (Momordica charantia) (BMO), which is rich in c9,t11,t13‐CLN, inhibited the occurrence of colonic aberrant crypt foci (ACF) induced by azoxymethane (AOM). In this study, we investigated the effect of dietary PGO on the development of AOM‐induced colonic malignancies and compared it with that of conjugated linoleic acid (CLA). To induce colonic tumors, 6‐week old male F344 rats were given subcutaneous injections of AOM (20 mg/kg body weight) once a week for 2 weeks. One week before the AOM treatment they were started on diet containing 0.01%, 0.1%, or 1%±PGO or 1% CLA for 32 weeks. Upon termination of the bioassay (32 weeks) colon tumors were evaluated histopathologically. AOM exposure produced colonic adenocarcinoma with an incidence of 81% and multiplicity of 1.88±1.54 at week 32. Administration of PGO in the diet significantly inhibited the incidence (AOM+0.01% PGO, 44%, P<0.05; AOM+0.1% PGO, 38%, P<0.01; AOM+1% PGO, 56%) and the multiplicity (AOM+0.01% PGO, 0.56±0.73, P<0<01; AOM+0.1% PGO, 0.50±0.73, P<0.005; AOM+1% PGO, 0.88±0.96, P<0.05) of colonic adenocarcinomas, although a clear dose‐response relationship was not observed at these dose levels. CLA feeding also slightly, but not significantly, reduced the incidence and multiplicity of colonic adenocarcinomas. The inhibition of colonic tumors by PGO was associated with an increased content of CLA (c9,t11–18:2) in the lipid fraction of colonic mucosa and liver. Also, administration of PGO in the diet elevated expression of peroxisome proliferator activated receptor (PPAR) γ protein in the nontumor mucosa. These results suggest that PGO rich in c9,t11,c13‐CLN can suppress AOM‐induced colon carcinogenesis, and the inhibition is associated in part with the increased content of CLA in the colon and liver and/or increased expression of PPARγ protein in the colon mucosa.
Publisher
Blackwell Publishing Ltd,Blackwell,John Wiley & Sons, Inc
Subject
/ Animals
/ Anticarcinogenic Agents - administration & dosage
/ Biological and medical sciences
/ Colon
/ Colonic Neoplasms - chemically induced
/ Colonic Neoplasms - prevention & control
/ Diet
/ Linolenic Acids - administration & dosage
/ Liver
/ Male
/ Mucosa
/ Oilseeds
/ Peroxisome proliferator-activated receptors
/ Plant Oils - administration & dosage
/ Rats
/ Receptors, Cytoplasmic and Nuclear - analysis
/ Seeds
/ Transcription Factors - analysis
/ Tumors
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