Iannone, Anna and Petroni, Anna and Murru, Maria Elisabetta and Cordeddu, Lina and Carta, Gianfranca and Melis, Maria Paola and Bergamini, Stefania and Della Casa, Lara and Cappiello, Laura and Carissimi, Romina and O’Shea, Marianne and Bell, Doris and De Santis, Enrico Pietro Luigi and Banni, Sebastiano (2009) Impairment of 8-iso-PGF2ALPHA isoprostane metabolism by dietary conjugated linoleic acid (CLA). Prostaglandins, Leukotrienes and Essential Fatty Acids, Vol. 80 (5-6), p. 279-287. eISSN 1532-2823. Article.
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8-iso-PGF2α isoprostane (IP) is one of the most-used markers of lipid peroxidation in experimental models and humans. After its formation, it is promptly metabolized to 2,3 dinor (DIN) in peroxisomes.
Conjugated linoleic acid (CLA) is preferentially β-oxidized in peroxisomes which may compete with IP, and thereby may affect its metabolism.
In order to verify whether CLA is able to influence IP formation and/or metabolism and to explain the mechanism, we challenged rats supplemented with CLA or with triolein (as a control fatty acid), with a single dose of carbon tetrachloride (CCl4) or of bacterial lipopolysaccharide (LPS). The results showed that IP and its precursor arachidonic acid hydroperoxide, as well as malondialdheyde (MDA), increase significantly in the liver of rats challenged with CCl4, irrespective of the diet, while in LPS-treated rats only nitrites in liver and isoprostane in plasma increase. On the other hand, the peroxisomal β-oxidation products of IP, the DIN, is significantly lower in the CLA group with respect to control and triolein groups.
To further investigate whether this is due to competition between CLA and IP at the cellular level, we incubated human fibroblasts from healthy subjects or patients with adrenoleukodystrophy (ALD), with CLA and/or commercially available IP. The rationale of this approach is based on the deficient peroxisomal β-oxidation of fibroblasts from ALD patients, leading to a reduced formation of DIN. In both normal and ALD cells, the presence of CLA significantly inhibits the formation of DIN from IP.
We may conclude that both in vitro and in vivo studies strongly suggest that CLA may impair IP catabolism in peroxisomes. Consequently an increase of IP, as a sole result of CLA intake, cannot be considered as a marker of lipid peroxidation.
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