Cited by 159Fatty Acid Research and HealthInflammatory mediators and NSAID effectsEdible Oils Quality and Analysis

Effects of fish oil on rectal cell proliferation, mucosal fatty acids, and prostaglandin e2 release in healthy subjects

Bartram, Hans-Peter, Gostner, Andrea, Scheppach, Wolfgang, Reddy, Bandaru S., Rao, Chinthalapally V., Dusel, Gerda, Richter, Frank, Richter, Astrid +1 more·1993·Gastroenterology

Abstract

Background Experimental studies have indicated dietary fish oil as a protective agent in colon carcinogenesis. Prostaglandins have been suggested to be involved in this process. In the present study, the effects of fish oil on rectal cell proliferation (i.e., intermediate biomarker of cancer risk), mucosal membrane fatty acids, and prostaglandin E2 (PGE2) release were investigated in 12 healthy volunteers.Methods In addition to a controlled basal diet, the test subjects received either fish oil (4.4 g omega-3 fatty acids/day) or corn oil supplements for two 4-week periods in a double-blind, crossover trial. Rectal cell proliferation was determined by bromodeoxyuridine immunohistochemistry and ornithine decarboxylase activity. After 2-hour incubation with bromodeoxyuridine, PGE2 concentration in the incubation medium was measured by radioimmunoassay. Mucosal membrane fatty acids were analyzed by gas chromatography.Results Bromodeoxyuridine labeling index (9.2% vs. 10.9%; P < 0.05), ornithine decarboxylase activity (19.7 vs. 36.4 pmol.mg protein-1.h-1; P < 0.005), and PGE2 release from rectal biopsy specimens (435.5 vs. 671.5 pg/mg wet tissue; P < 0.05) were significantly lower during the fish oil than the corn oil period, whereas membrane fatty acids were not statistically different.Conclusions The results support the hypothesis that dietary fish oil may protect against colon cancer.

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Crossref · 10.1016/0016-5085(93)90135-y

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  • EPA and DHA can inhibit endogenous production of pro-inflammatory arachidonic acids by competing as substrates for enzymes during eicosanoid synthesis.

    “EPA and DHA can also inhibit the endogenous production of pro-inflammatory arachidonic acids by competing as substrates for the enzymes during eicosanoid synthesis [66,67].”

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References 36 · Cited by 159

Authors
Bartram, H.-P., Gostner, A., Scheppach, W., Reddy, B. S., Rao, C. V., Dusel, G., Richter, F., Richter, A., & Kasper, H.
Affiliations
University of Würzburg (DE)
Venue
Gastroenterology
Publisher
Elsevier BV
Published
1993-11
Volume
105
Issue
5
Pages
1317-1322
ISSN
0016-5085 (ISSN-L)
OpenAlex
W2067664793
Cited by
159
References
36
Citations by year
2025: 2 · 2024: 3 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 2 · 2018: 5 · 2017: 5 · 2016: 2 · 2015: 3 · 2014: 3 · 2013: 9 · 2012: 8
FWCI
6.46
Type
journal article
Language
en
Open access
closed
Locations
  • Gastroenterology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Cancer Institute (NCI CA37663)
Topics
  • Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
  • Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
  • Physical Sciences › Chemistry › Organic Chemistry › Edible Oils Quality and Analysis
Keywords
fish oil, omega-3 fatty acids, prostaglandin E2, colon cancer chemoprevention, rectal mucosa, membrane fatty acids, ornithine decarboxylase, corn oil, dietary supplementation, cancer risk biomarkers
MeSH terms
Adult, Cell Division, Colonic Neoplasms, Corn Oil, Dietary Fats, Unsaturated, Double-Blind Method, Fatty Acids, Female, Fish Oils, Humans, Intestinal Mucosa, Male, Ornithine Decarboxylase, Rectum, Dinoprostone

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