Formation of the aldehydic choline glycerophospholipids in human red blood cell membrane peroxidized with an azo initiator.
The production of phospholipid hydroperoxide and aldehydic phospholipid was examined in human red blood cell (RBC) membranes after peroxidation with 2,2-azobis(2-amidinopropane)dihydrochloride (AAPH) or xanthine/xanthine oxidase (XO/XOD/Fe3+). Both radical-generation systems caused a profound decrease in the amount of polyunsaturated fatty acid (PUFA) in choline glycerophospholipid (CGP) and induced formation of peroxidized CGP in RBC membranes to different extents. No consistent generation of peroxidized lipids from CGP was evident after peroxidation with XO/XOD/Fe3+, which caused the apparent decomposition of phospholipids and the formation of large amounts of thiobarbituric acid-reactive substance (TBARS). On the other hand, CGP hydroperoxide was formed as a primary product of peroxidation with AAPH. Aldehydic CGP was also detected as a secondary product of hydroperoxide decomposition in AAPH-peroxidized RBC membranes. Aldehydic CGP was preferentially generated from arachidonoyl CGP rather than from linoleoyl CGP in AAPH-peroxidized membranes. AAPH mainly oxidized CGP to hydroperoxide and aldehydic phospholipids. The sum of hydroperoxide and aldehyde of CGP corresponded to the loss of CGP due to peroxidation by AAPH. This result indicates that CGP was mainly converted into these two oxidized phospholipids in AAPH-peroxidized RBC membranes.
Kawai
Y
Y
School of Pharmaceutical Sciences, Kitasato University, Minato-ku, Tokyo, 108-8641, Japan.
Ogamo
A
A
Nakagawa
Y
Y
D000447:Aldehydes / Q000378:metabolism; D000578:Amidines / Q000494:pharmacology*; D002851:Chromatography, High Pressure Liquid / Q000379:methods; D004910:Erythrocyte Membrane / Q000187:drug effects / Q000378:metabolism*; D005231:Fatty Acids, Unsaturated / Q000032:analysis / Q000378:metabolism; D005609:Free Radicals; D020404:Glycerophospholipids / Q000737:chemistry / Q000378:metabolism*; D005997:Glycerylphosphorylcholine / Q000378:metabolism; D006801:Humans; D017665:Hydroxyl Radical; D007501:Iron / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects*; D008054:Lipid Peroxides / Q000378:metabolism*; D010069:Oxadiazoles / Q000737:chemistry; D016877:Oxidants / Q000494:pharmacology; D010084:Oxidation-Reduction; D013449:Sulfonamides / Q000737:chemistry; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D019820:Xanthine / Q000378:metabolism; D014969:Xanthine Oxidase / Q000378:metabolism
D000447:Aldehydes; D000578:Amidines; D005231:Fatty Acids, Unsaturated; D005609:Free Radicals; D020404:Glycerophospholipids; D008054:Lipid Peroxides; D010069:Oxadiazoles; D016877:Oxidants; D013449:Sulfonamides; D017392:Thiobarbituric Acid Reactive Substances; C080612:4-(N,N-dimethylaminosulfonyl)-7-hydrazino-2,1,3-benzoxadiazole; D019820:Xanthine; D017665:Hydroxyl Radical; D005997:Glycerylphosphorylcholine; C046728:2,2'-azobis(2-amidinopropane); D007501:Iron; D014969:Xanthine Oxidase