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Differential efficiency of lysophospholipid markers for oxidative stress
Author(s) -
Schober Celestina,
Fuchs Beate,
Schiller Jürgen
Publication year - 2009
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.23.1_supplement.871.4
Subject(s) - lysophosphatidylcholine , hypochlorous acid , phosphatidylethanolamine , chemistry , polyunsaturated fatty acid , phosphatidylserine , oxidative stress , plasmalogen , phosphatidylcholine , biochemistry , myeloperoxidase , inflammation , phospholipid , fatty acid , biology , immunology , membrane
Inflammatory liver diseases are associated with marked oxidative stress. At inflammatory loci, hypochlorous acid (HOCl) is generated by myeloperoxidase. HOCl reacts with a variety of molecules and induces the formation of lysophosphatidylcholine (LPC) from polyunsaturated phosphatidylcholine (PC). Since liver tissue contains huge amounts of polyunsaturated PC the arising of enhanced LPC concentrations could be expected and was experimentally verified in various species. Surprisingly, further lysophospholipids (LPL) could not be detected, although human liver contains many further polyunsaturated phospholipid (PL) classes. Therefore, four different isolated PL classes were investigated regarding the extent of LPL generation under the influence of HOCl. Using MALDI‐TOF mass spectrometry (MS) PC could be identified as the only PL leading to LPC, whereas phosphatidylglycerol, phosphatidylserine and phosphatidylethanolamine led exclusively to chlorohydrins by the reaction of HOCl with the double bonds of their unsaturated fatty acyl residues. Thus, LPC represents a useful biomarker of oxidative stress and inflammation that can be easily determined by MS ‐ even in complex mixtures.