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Metabolism of 8‐iso‐PGF2alpha and conjugated linoleic acid (CLA) in vivo and in X‐Adrenoleukodystrophy fibroblasts
Author(s) -
Petroni Anna,
Ian Carla Anna,
Cordeddu Lina,
Murru Elisabetta,
Carta Gianfranca,
Melis Maria Paola,
Bergamini Stefania,
Blasevich Milena,
Carissimi Romina,
O'Shea Marianne,
De Santis Enrico,
Banni Sebastiano
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a23-c
Subject(s) - adrenoleukodystrophy , conjugated linoleic acid , peroxisome , chemistry , in vivo , linoleic acid , metabolism , arachidonic acid , medicine , oxidative stress , endocrinology , biochemistry , fatty acid , biology , enzyme , receptor , microbiology and biotechnology
X‐adrenoleukodystrophy (X‐ALD) is an inherited neurodegenerative disorder characterized by impaired peroxisomal beta‐oxidation. It has been shown that conjugated linoleic acid (CLA) intake in humans increased plasma levels of isoprostanes . This increase has been taken as an evidence of oxidative stress triggered by CLA. This compound and 8‐iso‐PGF2alpha (IP), have peroxisomal bet‐oxidation. The aim of our study was to investigate the metabolism of CLA and its influence on IP formation, in vivo and in fibroblasts from X‐ALD. We challenged rats fed CLA with a single dose of CCl4. The results showed that IP and its precursor arachidonic acid hydroperoxides increased significantly in the liver of rats challenged with CCl4. On the other hand, the peroxisomal beta oxidation products of IP, diinor (DIN), was found only in the free form and significantly lower in the CLA group with respect to the control groups. To further investigate whether there is a competition between CLA and IP at cellular level, we incubated human fibroblasts from healthy subjects or patients affected by X‐ALD with CLA and/or commercially available IP. In X‐ALD fibroblasts the formation of DIN was significantly lower, in both normal and ALD cells, the presence of CLA significantly inhibited the formation of DIN from IP.