Submitted on July 26, 2006
Revised on December 18, 2006
Accepted on January 11, 2007
Evidence for in situ ethanolamine phospholipid adducts with hydroxy-alkenals
Sandrine Bacot, Nathalie Bernoud-Hubac, Bernard Chantegrel, Christian Deshayes, Alain Doutheau, Gabriel Ponsin, Michel Lagarde, and Michel Guichardant
Biochemistry, INSERM UMR 585 / INSA-Lyon, Villeurbanne 69621
Corresponding Author: Michel.Guichardant{at}insa-lyon.fr
Hydroxy-alkenals, such as 4-hydroxy-nonenal (4-HNE) (from n-6 fatty acids), are degradation products of fatty acid hydroperoxides, including those generated by free radical attack of membrane polyunsaturated fatty acyl moieties. The cytotoxic effects of hydroxy-alkenals are well known, and mainly due to their interaction with different molecules to form covalent adducts. Indeed, ethanolamine phospholipids (PE) can be covalently modified in a cellular system by hydroxy-alkenals, such as 4-HNE, 4-hydroxy-hexenal (4-HHE) (from n-3 fatty acids) and 4-hydroxy-dodecadienal (4-HDDE) (from the 12-lipoxygenase product of arachidonic acid), to form mainly Michael adducts. In the present study, we describe the formation of ethanolamine phospholipid Michael adducts in human blood platelets in response to oxidative stress, and in retinas of streptozotocin-induced diabetic rats. We have successfully characterized and evaluated, for the first time, ethanolamine phospholipids coupled with 4-HHE, 4-HNE and 4-HDDE by gas chromatography–mass spectrometry measurement of their ethanolamine moities. We also report that aggregation of isolated human blood platelets enriched with PE-4-hydroxy-alkenals Michael adducts was altered. These data suggest that these adducts could be used as specific markers of membrane disorders occurring in pathophysiological states with associated oxidative stress, and might affect cell function.
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