Effects of fish oil on rectal cell proliferation, mucosal fatty acids, and prostaglandin E2 release in healthy subjects

Bartram, H.; Gostner, Andrea; Scheppach, Wolfgang; Reddy, Bandaru S.; Rao, Chinthalapally V.; Dusel, Gerda; Richter, Frank; Richter, Anna; Kasper, Heinrich

doi:10.1016/0016-5085(93)90135-y

Cited by 148 publications

(70 citation statements)

References 23 publications

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“…Our study is one of the first to report on the in vitro effects of FAs on normal human adult epithelial cells and our observations suggest that there are marked similarities in the responses to FAs of normal proliferating epithelial cells compared with studies involving carcinoma-derived cell lines. This is in agreement with studies of the effects of dietary FAs on proliferation of normal cells in vivo, which have also demonstrated that diets high in PUFAs can be anti-mitotic for the normally rapidly proliferating epithelial cells in intestinal crypts (Anti et al, 1992;Bartram et al, 1993;Pell et al, 1994).…”

Section: Discussionsupporting

confidence: 91%

“…As noted above, the in vivo data would suggest that diets high in fish oils might protect against tumour development (Anti et al, 1992) and growth (Narisawa et al, 1994) and can inhibit normal epithelial cell proliferation in colonic crypts (Bartram et al, 1993;Pell et al, 1994). Although the effects of fish oils have been attributed to the n-3 PUFAs, it must be remembered that fish oils typically contain less than 50% of n-3 PUFAs and it has been pointed out that care should be taken when attributing effects to single fatty acids when complex mixtures of oils are administered (Garton, 1992).…”

Section: Discussionmentioning

confidence: 96%

“…On the basis of animal studies, several hypotheses have been put forward to explain why polyunsaturated n-3 FAs might be tumour suppressive, including reduced sensitivity to tumour promoters as a consequence of changes in membrane lipid composition (Narisawa et al, 1991). It has also been shown that a n-3 PUFA-rich diet can reduce the proliferation rate of normal colonic crypt epithelial cells (Anti et al, 1992;Bartram et al, 1993;Pell et al, 1994). As reduced normal cell proliferation may confer protection against the development of cancer (Preston-Martin et al, 1990), this raises the intriguing possibility that PUFAs may be inhibitory to all rapidly proliferating epithelial cells, rather than just malignantly transformed carcinoma cells.…”

mentioning

confidence: 99%

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The effects of dietary fatty acids on the proliferation of normal human urothelial cells in vitro

Southgate

Pitt²,

Trejdosiewicz³

1996

Br J Cancer

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Summary Little is known of the mechanisms by which dietary fatty acids (FAs) may affect normal epithelial cell physiology and thereby directly or indirectly influence tumour incidence and progression. In this study, we have used normal human urothelial cell cultures to investigate whether FAs may modify proliferation of normal human epithelial cells in vitro. FAs were presented as albumin complexes in serum-free medium and the effects on proliferation over a concentration range of 1-100 gM were assayed by thymidine incorporation.Saturated FAs had no effect. At lower concentrations (1-10 gM), mono-unsaturated FAs (MUFAs) and n-3 polyunsaturated FAs (PUFAs) were slightly stimulatory. Concentrations of unsaturated FAs above 10 pm were growth inhibitory in a dose-dependent manner. Oleic acid showed least cytostatic effect, whereas y-linolenic acid induced irreversible growth arrest. Although marked morphological effects were observed in irreversibly growth-inhibited cells, the cells remained attached to the substratum and showed no evidence of nuclear pyknosis or apoptosis. The inhibitory effects of single PUFAs could be reduced, but not abolished, by the addition of saturated FAs or MUFAs. Mixtures of different PUFAs were inhibitory in an additive manner. These data suggest that PUFAs have a cytostatic effect on rapidly proliferating epithelial cells which appears unrelated to malignant transformation.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 99%

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The effects of dietary fatty acids on the proliferation of normal human urothelial cells in vitro

Southgate

Pitt²,

Trejdosiewicz³

1996

Br J Cancer

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“…When n-3 fatty acids are consumed in the diet, eicosapentanoic acid, which is the substrate for synthesis of n-3 derived eicosanoids such as PGE 3 and TXA 3 , is proportionately increased in the phospholipids of cellular membranes (Anti et al, 1992) while arachidonic acid, which is the substrate for synthesis of n-6 derived eicosanoids such as PGE 2 and TXA 2 , is decreased. Indeed, as little as 4.4 g of n-3 fatty acids per day significantly increased EPA, decreased arachidonic acid and decreased the PGE 2 in colonic mucosa of healthy volunteers (Bartram et al, 1993). Thus suppression of PGE 2 and TXA 2 synthesis by consumption of dietary n-3 FA would be expected to decrease the diarrhoea induced by eicosanoid mediated Cl-secretion and would be expected to decrease the diarrhoea associated with CPT-11 treatment.…”

Section: Relevance Of Fish Oil Supplementation On Prostaglandin Synthmentioning

confidence: 95%

Fish oil supplementation enhanced CPT-11 (irinotecan) efficacy against MCF7 breast carcinoma xenografts and ameliorated intestinal side-effects

1999

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SummaryThe cancer chemotherapeutic efficacy of the topoisomerase I inhibitor, is often limited by the induction of severe delayed diarrhoea. In animal studies, CPT-11 use is associated with histopathological damage to the mucosa of the small and large intestines. Results from the present study demonstrate that 60 mg CPT-11 per kg body weight (i.v. q4d ϫ 6) halted the growth, but did not cause significant regression, of MCF7 human breast carcinoma xenografts in mice fed a diet containing 7% corn oil. However, when the diet of the MCF7-bearing mice was supplemented with 3% or 6% fish oil, the same CPT-11 treatment caused significant regression of the MCF7 xenograft. Histomorphometric analyses of intestinal mucosa of mice treated with CPT-11 and fed the diet containing 7% corn oil indicated that treatment with CPT-11 induced structural changes in the intestinal mucosa which persisted at least 5 days after the last dose of CPT-11. The intestinal mucosal architecture of mice that were treated with CPT-11 and fed the diets containing fish oil was largely unchanged from the architecture of the group of mice which did not receive CPT-11. These findings indicate that fish oil supplements may be a useful adjunct to CPT-11 treatment.

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“…Omega-3 fatty acids have been shown to slow cell proliferation in normal tissues (Anti et al, 1994;Bartram et al, 1993;Calviello et al, 1999;Meydani et al, 1991) thus the observed reduction in the number of micronuclei in peripheral erythrocytes and in the number of apoptotic figures in the duodenal crypts of mice treated with CPT-11 and fed AAFA TM may simply be due to slower proliferation during the time of CPT-11 treatment. The fact that we observed less apoptosis in the crypt columns of the mice yet the number of cells in each crypt column was not changed also indicates that proliferation in the intestinal mucosa was slowed due to AAFA TM consumption.…”

Section: Experimental Therapeuticsmentioning

confidence: 99%

Consumption of an omega-3 fatty acids product, INCELL AAFA™, reduced side-effects of CPT-11 (irinotecan) in mice

2002

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INCELL AAFATM , an omega-3 polyunsaturated fatty acid product containing a high concentration of long chain fatty acids, was tested for its ability to ameliorate the harmful side effects of CPT-11 chemotherapy including: leukopenia, anaemia, asthenia, weight loss and liver involvement. Four groups of mice were fed an AIN-76 diet modified to contain: 10% w/w corn oil (CO), 0% AAFA TM ; 9% CO, 1% AAFA TM ; 8% CO, 2% AAFA TM ; or 7% CO, 3% AAFA TM . After 2 weeks on the diets, half of the mice received CPT-11 chemotherapy (60 mg kg 71 q 4 days, i.v.) the rest of the mice received vehicle for 2 weeks. It was found that 2% AAFA TM in the diet of the CPT-11 treated mice: decreased apoptotic figures in the duodenal crypts; markedly suppressed the inflammatory eicosanoid, prostaglandin E 2 in the liver; prevented liver hypertrophy; improved white blood cell counts; significantly increased red blood cell counts; decreased numbers of CPT-11 induced immature red blood cell and micronuclei in red blood cells of the peripheral blood; increased eicosapentaenoic acid and docosahexaenoic acid in liver cell membranes and maintained normal grooming behaviour. Thus 2% AAFA TM in the diet reduced the side effects of CPT-11 treatment in mice.

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Effects of fish oil on rectal cell proliferation, mucosal fatty acids, and prostaglandin E2 release in healthy subjects

Cited by 148 publications

References 23 publications

The effects of dietary fatty acids on the proliferation of normal human urothelial cells in vitro

The effects of dietary fatty acids on the proliferation of normal human urothelial cells in vitro

Fish oil supplementation enhanced CPT-11 (irinotecan) efficacy against MCF7 breast carcinoma xenografts and ameliorated intestinal side-effects

Consumption of an omega-3 fatty acids product, INCELL AAFA™, reduced side-effects of CPT-11 (irinotecan) in mice

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