Abstract
Hydroxy-alkenals, such as 4-hydroxy-2(E)-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 are mainly attributable to their interaction with different molecules to form covalent adducts. Indeed, ethanolamine phospholipids (PEs) can be covalently modified in a cellular system by hydroxy-alkenals, such as 4-HNE, 4-hydroxy-2(E)-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 this study, we describe the formation of PE 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, PEs coupled with 4-HHE, 4-HNE, and 4-HDDE by gas chromatography-mass spectrometry measurement of their ethanolamine moieties. We also report that aggregation of isolated human blood platelets enriched with PE-4-hydroxy-alkenal 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.
Highlights
Hydroxy-alkenals, such as 4-hydroxy-2(E )-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 first aim of this study was to investigate the occurrence of such Michael adducts formed between PEs and the above-mentioned aldehydes in oxidative stress conditions, induced either in human blood platelets in vitro or Abbreviations: AA, arachidonic acid; DHA, docosahexaenoic acid; 4-HDDE, 4-hydroxy-2(E),6(Z)-dodecadienal; 4-HHE, 4-hydroxy-2(E)hexenal; 4-HNE, 4-hydroxy-2(E)-nonenal; NICI, negative ion chemical ionization; PE, ethanolamine phospholipid; PRP, platelet-rich plasma; SIM, selected ion monitoring; TFAI, 1-(trifluoroacetyl)imidazole
The derivatized ethanolamine adducts were eluted at 17.34, 18.80, and 20.73 min, respectively. Their mass spectra (Fig. 2) showed that ions at m/z 561, 603, and 643 correspond to the molecular anion radicals [M]I2 of the ethanolamine moiety modified by 4-HHE, 4-HNE, and 4-HDDE, respectively
Summary
Hydroxy-alkenals, such as 4-hydroxy-2(E )-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. Ethanolamine phospholipids (PEs) can be covalently modified in a cellular system by hydroxy-alkenals, such as 4-HNE, 4-hydroxy-2(E)-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. We describe the formation of PE Michael adducts in human blood platelets in response to oxidative stress and in retinas of streptozotocin-induced diabetic rats. The first aim of this study was to investigate the occurrence of such Michael adducts formed between PEs and the above-mentioned aldehydes in oxidative stress conditions, induced either in human blood platelets in vitro or Abbreviations: AA, arachidonic acid; DHA, docosahexaenoic acid; 4-HDDE, 4-hydroxy-2(E),6(Z)-dodecadienal; 4-HHE, 4-hydroxy-2(E)hexenal; 4-HNE, 4-hydroxy-2(E)-nonenal; NICI, negative ion chemical ionization; PE, ethanolamine phospholipid; PRP, platelet-rich plasma; SIM, selected ion monitoring; TFAI, 1-(trifluoroacetyl)imidazole. We have explored the biological effect of PE-4-HNE Michael adduct on human blood platelet aggregation
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