Effects of dietary conjugated linoleic acid on DNA adduct formation of PhIP and IQ after bolus administration to female F344 rats

Josyula, Shylaja; Schut, Herman A.J.

doi:10.1080/01635589809514732

Cited by 19 publications

(4 citation statements)

References 32 publications

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“…Previous studies have shown that CLA does not alter CYP expression. 43,44) However, it is possible that PGO may affect liver CYPs, including CYP2E1, which activates AOM, since dietary CLN suppressed AOM-induced ACF when fed during AOM exposure. 25) The results described here suggest that dietary feeding of PGO suppressed progression of these lesions through adenoma to malignant neoplasm in the post-initiation phase.…”

Section: Discussionmentioning

confidence: 99%

Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats

et al. 2004

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Pomegranate (Punica granatum L.) seed oil (PGO) contains more than 70% cis(c)9,trans(t)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 ( olon cancer is one of the leading causes of cancer deaths in Western countries. Globally, more than 875,000 men and women were afflicted with this cancer in 1996 and more than 510,000 died in the same year.

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Section: Discussionmentioning

confidence: 99%

Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats

et al. 2004

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“…A number of studies have reported a protective activity of CLA against HCA-induced carcinogenesis by measuring changes in HCA-DNA adduct levels. CLA was found to reduce the formation of PhIP-DNA adducts in the colon, 2-amino-3-methylimidazo[4,5-f]quinoline (IQ)-DNA adducts in the mammary gland of female rats [Josyula and Schut 1998], and DNA adducts and aberrant crypt foci induced by IQ in the colon of male rats [Liew et al, 1995]. Of particular interest is that the protective efficacy of CLA is sex-related, as shown by Zu and Schut [1992].…”

Section: Introductionmentioning

confidence: 98%

Sex‐specific induction of mutations by PhIP in the kidney of male and female rats and its modulation by conjugated linoleic acid

Yang

Glickman

Boer

2002

Environ and Mol Mutagen

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The heterocyclic amine 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a recognized mutagen and carcinogen in the colon and prostate of male rats and in the mammary gland of female rats. In the current study, we examined the mutagenicity of PhIP in the kidney of male and female lacI transgenic rats and its modulation by a dietary chemopreventive agent, conjugated linoleic acid (CLA). Sex-specific changes in mutation were observed following PhIP and CLA treatment. Exposure to 100 ppm PhIP through dietary supplementation for 47 days induced a lacI mutation frequency (MF) of 7.7 +/- 0.3 x 10(-5) and 4.7 +/- 1.0 x 10(-5) in the kidney of male and female rats, respectively. The PhIP-induced MFs in the kidney of male and female rats were significantly different from each other and were 300% (P < 0.001) and 60% (P < 0.05) higher than the corresponding controls, respectively. When rats were given CLA along with PhIP, CLA completely inhibited the formation of PhIP-induced mutations in the kidney of female rats, but not in male rats. Comparison of mutational spectra did not detect significant differences between male rats treated with PhIP and PhIP + CLA. However, unlike the -1 frameshifts induced by PhIP in the colon and prostate, which consist primarily of G:C deletions, -1 frameshifts in the kidney involved the loss of both G:C and A:T basepairs. Our data indicate that the kidney of the rats responds in a sex-dependent way to mutagenesis and antimutagenesis by PhIP and CLA. These differences may be related to hormonally regulated induction of P450 enzymes or cell proliferation.

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“…Presumably, chemical compounds responsible for activation of CYP 1A1/1A2 in the liver and intestine enter the body with food [10] or were formed in the gastrointestinal tract as a result of vital activity of some bacteria.…”

Section: Resultsmentioning

confidence: 99%

Basal induction of cytochrome P-450 1A1/1A2 in cells of the liver, small intestinal villi, and lymph nodes in rats

et al. 2006

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Rat liver, small intestinal wall, mesenteric, mediastinal, and popliteal lymph nodes of rats were studied by indirect immunoperoxidase method with monoclonal antibodies to cytochrome P-450 1A1/1A2. These cytochrome forms were detected in low concentrations in hepatocytes, macrophages of the small intestinal villi and mesenteric and mediastinal lymph nodes of intact animals. Basal induction of monooxygenase enzymes can be caused by cytochrome inductors entering with air (environmental pollution) or food.

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Effects of dietary conjugated linoleic acid on DNA adduct formation of PhIP and IQ after bolus administration to female F344 rats

Cited by 19 publications

References 32 publications

Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats

Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats

Sex‐specific induction of mutations by PhIP in the kidney of male and female rats and its modulation by conjugated linoleic acid

Basal induction of cytochrome P-450 1A1/1A2 in cells of the liver, small intestinal villi, and lymph nodes in rats

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