Metabolic and ultrastructural changes in articular cartilage of rats fed dietary supplements of omega‐3 fatty acids

A “marginally deficient” essential fatty acid state was produced in male Sprague‐Dawley rats by dietary supplementation with Ω3 fatty acids. Animals fed diets containing the highest amounts of these fatty acids (10% menhaden fish oil) demonstrated a 70% maximum decrease in the linoleic and arachidon...

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Veröffentlicht in:Arthritis and rheumatism 1990-07, Vol.33 (7), p.1029-1036
Hauptverfasser: Lippiello, Louis, Fienhold, Margery, Grandjean, Carter
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Sprache:eng
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Zusammenfassung:A “marginally deficient” essential fatty acid state was produced in male Sprague‐Dawley rats by dietary supplementation with Ω3 fatty acids. Animals fed diets containing the highest amounts of these fatty acids (10% menhaden fish oil) demonstrated a 70% maximum decrease in the linoleic and arachidonic acid content of articular cartilage, a 30–40% decrease in cartilage hexosamine content, with little effect on hydroxyproline levels, and a 32% inhibition of proteoglycan synthesis. Histologic analysis revealed an occasional surface irregularity and localized depletion of Safranin O and toluidine blue staining of articular cartilage on the femoral heads from animals taking the higher doses. Electron microscopic analysis revealed a marked decrease in “dark‐staining” chondrocytes relative to “light‐staining” cells in all animals fed menhaden fish oil. The cartilaginous changes noted in this study reflect a causal relationship between chondrocyte metabolism and an altered unsaturated fatty acid content. The observed responses of chondrocytes to Ω3 fatty acids may be similar to those commonly associated with the development of early osteoarthrosis. It is not known whether similar changes are induced in other species, including humans, but these observations suggest that some caution must be taken in the long‐term adminitration of menhaden fish oil or other Ω3 fatty acid‐containing preparations in rheumatoid arthritis patients.
ISSN:0004-3591
1529-0131
DOI:10.1002/art.1780330716