Lipid oxidation is implicated in a wide range of pathophysiogical disorders, and leads to reactive compounds such as fatty aldehydes, of which the most well known is 4-hydroxy-2E-nonenal (4-HNE) issued from 15-hydroperoxyeicosatetraenoic acid (15-HpETE), an arachidonic acid (AA) product. In addition to 15-HpETE, 12(S)-HpETE is synthesized by 12-lipoxygenation of platelet AA. We first show that 12-HpETE can be degraded in vitro into 4-hydroxydodeca-(2E,6Z)-dienal (4-HDDE), a specific aldehyde homologous to 4-HNE. Moreover, 4-HDDE can be detected in human plasma. Second, we compare the ability of 4-HNE, 4-HDDE, and 4-hydroxy-2E-hexenal (4-HHE) from n-3 fatty acids to covalently modify different ethanolamine phospholipids (PEs) chosen for their biological relevance, namely AA- (20: 4n-6) or docosahexaenoic acid- (22:6n-3) containing diacyl-glycerophosphoethanolamine (diacyl-GPE) and alkenylacyl-glycerophosphoethanolamine (alkenylacyl-GPE) molecular species. The most hydrophobic aldehyde used, 4-HDDE, generates more adducts with the PE subclasses than does 4-HNE, which itself appears more reactive than 4-HHE. Moreover, the aldehydes show higher reactivity toward alkenylacyl-GPE compared with diacyl-GPE, because the docosahexaenoyl-containing species are more reactive than those containing arachidonoyl.We conclude that the different PE species are differently targeted by fatty aldehydes: the higher their hydrophobicity, the higher the amount of adducts made. In addition to their antioxidant potential, alkenylacyl-GPEs may efficiently scavenge fatty aldehydes. Lipid oxidation is implicated in a wide range of pathophysiogical disorders, and leads to reactive compounds such as fatty aldehydes, of which the most well known is 4-hydroxy-2E-nonenal (4-HNE) issued from 15-hydroperoxyeicosatetraenoic acid (15-HpETE), an arachidonic acid (AA) product. In addition to 15-HpETE, 12(S)-HpETE is synthesized by 12-lipoxygenation of platelet AA. We first show that 12-HpETE can be degraded in vitro into 4-hydroxydodeca-(2E,6Z)-dienal (4-HDDE), a specific aldehyde homologous to 4-HNE. Moreover, 4-HDDE can be detected in human plasma. Second, we compare the ability of 4-HNE, 4-HDDE, and 4-hydroxy-2E-hexenal (4-HHE) from n-3 fatty acids to covalently modify different ethanolamine phospholipids (PEs) chosen for their biological relevance, namely AA- (20: 4n-6) or docosahexaenoic acid- (22:6n-3) containing diacyl-glycerophosphoethanolamine (diacyl-GPE) and alkenylacyl-glycerophosphoethanolamine (alkenylacyl-GPE) molecular species. The most hydrophobic aldehyde used, 4-HDDE, generates more adducts with the PE subclasses than does 4-HNE, which itself appears more reactive than 4-HHE. Moreover, the aldehydes show higher reactivity toward alkenylacyl-GPE compared with diacyl-GPE, because the docosahexaenoyl-containing species are more reactive than those containing arachidonoyl. We conclude that the different PE species are differently targeted by fatty aldehydes: the higher their hydrophobicity, the higher the amount of adducts made. In addition to their antioxidant potential, alkenylacyl-GPEs may efficiently scavenge fatty aldehydes. Ethanolamine phospholipids (PEs) in biological membranes consist of two main subclasses: diacyl-glycerophosphoethanolamine (diacyl-GPE) and alkenylacyl-glycerophosphoethanolamine (alkenylacyl-GPE). The brain is particularly rich in plasmalogens, a unique class of glycerophospholipids exhibiting antioxidant properties due to the presence of a vinyl ether moiety at the sn-1 position of the glycerol backbone. The sn-2 position is acylated primarily by PUFAs such as arachidonic acid (AA) (20:4n-6) and docosahexaenoic acid (DHA) (22:6n-3). Plasmalogens represent 15–20% of total phospholipids (1Sun G.Y. Horrocks L.A. Acyl and alk-1-enyl group compositions of the alk-1′-enyl acyl and the diacyl glycerophosphorylethanolamines of mouse and ox brain.J. Lipid. Res. 1969; 10: 153-157Google Scholar, 2Horrocks L.A. Ether Lipids. Chemistry and Biology.in: Snyder F. Academic Press, New York1972: 177-272Google Scholar, 3Favreliere S. Barrier L. Durand G. Chalon S. Tallineau C. Chronic dietary n-3 polyunsaturated fatty acids deficiency affects the fatty acid composition of plasmenylethanolamine and phosphatidylethanolamine differently in rat frontal cortex, striatum, and cerebellum.Lipids. 1998; 33: 401-407Google Scholar) and more than 50% of PEs (4Favreliere S. Stadelmann-Ingrand S. Huguet F. De Javel D. Piriou A. Tallineau C. Durand G. Age-related changes in ethanolamine glycerophospholipid fatty acid levels in rat frontal cortex and hippocampus.Neurobiol. Aging. 2000; 21: 653-660Google Scholar). Cell antioxidant defenses such as glutathione peroxidases (GPx), superoxide dismutase, or vitamins E and C prevent and/or scavenge highly reactive oxygen species (ROS) (5Zoeller R.A. Morand O.H. Raetz C.R. A possible role for plasmalogens in protecting animal cells against photosensitized killing.J. Biol. Chem. 1988; 263: 11590-11596Google Scholar, 6Zommara M. Tachibana N. Mitsui K. Sakono M. Ikeda I. Imaizumi K. Inhibitory effect of ethanolamine plasmalogen on iron and copper-dependent lipid peroxidation.Free Radic. Biol. Med. 1995; 18: 599-602Google Scholar, 7Reiss D. Beyer K. Engelmann B. Delayed oxidative degradation of polyunsaturated diacyl phospholipids in the presence of plasmalogen phospholipids in vitro.Biochem. J. 1997; 323: 807-814Google Scholar, 8Sindelar P.J. Guan Z. Dallner G. Ernster L. The protective role of plasmalogens in iron-induced lipid peroxidation.Free Radic. Biol. Med. 1999; 26: 318-324Google Scholar). Uncontrolled formation of ROS leads to oxidative stress, responsible for lipid peroxidation, which generates lipid hydroperoxides. The latter compounds are normally reduced into monohydroxylated fatty acids by GPx (9Bryant R.W. Bailey J.M. Altered lipoxygenase metabolism and decreased glutathione peroxydase activity in platelets from selenium deficient rats.Biochem. Biophys. Res. Commun. 1980; 92: 268-276Google Scholar), but oxidative stress conditions in which GPx activities may be decreased, such as in aging and diabetes (10Vericel E. Rey C. Calzada C. Haond P. Chapuy P.H. Lagarde M. Age-related changes in arachidonic acid peroxidation and glutathione-peroxidase activity in human platelets.Prostaglandins. 1992; 43: 75-85Google Scholar, 11Muruganandam A. Drouillard C. Thibert R.J. Cheung R.M. Draisey T.F. Mutus B. Glutathione metabolic enzyme activities in diabetic platelets as a function of glycemic control.Thromb. Res. 1992; 67: 385-397Google Scholar), favor the accumulation of hydroperoxides. The breakdown of these compounds generates a variety of products, such as aldehydes, of which 4-hydroxy-2E-nonenal (4-HNE) has been widely investigated. 4-HNE is produced from the most abundant n-6 PUFA-derived hydroperoxides, namely 15-hydroperoxyeicosatetraenoic acid(15-HpETE) and 13-hydroperoxy-linoleic acid (12Esterbauer H. McBrien D.C.H. Slater T.F. Aldehydic Products of Lipid Peroxidation: Free Radicals Lipid Peroxidation and Cancer. Academic Press, London1982: 101-128Google Scholar, 13Poli G. Dianzani M.U. Cheeseman K.H. Slater T.F. Lang J. Esterbauer H. Separation and characterization of the aldehydic products of lipid peroxidation stimulated by carbon tetrachloride or ADP-iron in isolated rat hepatocytes and rat liver microsomal suspensions.Biochem. J. 1985; 227: 629-638Google Scholar). Although the breakdown of 15-HpETE has been well described, that of 12-HpETE, the 12-lipoxygenase product of AA, remains partially unknown. The putative 12-HpETE-derived aldehyde, 4-hydroxydodeca-(2E,6Z)-dienal (4-HDDE) was characterized in the present study and measured in human plasma. Also, 4-hydroxy-2E-hexenal (4-HHE) is described as a major degradation product of n-3 PUFA peroxidation, such as DHA (14Van Kuijk F.J. Holte L.L. Dratz E.A. 4-Hydroxyhexenal: a lipid peroxidation product derived from oxidized docosahexaenoic acid.Biochim. Biophys. Acta. 1990; 1043: 116-118Google Scholar). 4-HNE is produced in many degenerative diseases, such as atherosclerosis (15Vieira O. Escargueil-Blanc I. Jurgens G. Borner C. Almeida L. Salvayre R. Negre-Salvayre A. Oxidized LDLs alter the activity of the ubiquitin-proteasome pathway: potential role in oxidized LDL-induced apoptosis.FASEB J. 2000; 14: 532-542Google Scholar), diabetes (16Al Abed Y. Liebich H. Voelter W. Bucala R. Hydroxyalkenal formation induced by advanced glycosylation of low density lipoprotein.J. Biol. Chem. 1996; 271: 2892-2896Google Scholar), inflammation (17Grune T. Siems W.G. Schönheit K. Blasig I.E. Release of 4-hydroxynonenal, an aldehydic mediator of inflammation, during postischaemic reperfusion of the myocardium.Int. J. Tissue React. 1993; 15: 145-150Google Scholar, 18Di Mauro C. Cavalli G. Curzio M. Ferretti C. Mengozzi G. Rossi M.A. Paradisi L. Dianzani M.U. Evidences of 4-hydroxynonenal involvement in modulation of phagocyte activities.Int. J. Tissue React. 1995; 17: 61-72Google Scholar, 19Hamilton Jr., R.F. Li L. Eschenbacher W.L. Szweda L. Holian A. Potential involvement of 4-hydroxynonenal in the response of human lung cells to ozone.Am. J. Physiol. 1998; 274: L8-L16Google Scholar), and neurodegenerative diseases (20Montine K.S. Kim P.J. Olson S.J. Markesbery W.R. Montine T.J. 4-Hydroxy-2-nonenal pyrrole adducts in human neurodegenerative disease.J. Neuropathol. Exp. Neurol. 1997; 56: 866-871Google Scholar, 21Odetti P. Garibaldi S. Norese R. Angelini G. Marinelli L. Valentini S. Menini S. Traverso N. Zaccheo D. Siedlak S. Perry G. Smith M.A. Tabaton M. Lipoperoxidation is selectively involved in progressive supranuclear palsy.J. Neuropathol. Exp. Neurol. 2000; 59: 393-397Google Scholar) such as Alzheimer’s disease (22Lovell M.A. Ehmann W.D. Mattson M.P. Markesbery W.R. Elevated 4-hydroxynonenal in ventricular fluid in Alzheimer’s disease.Neurobiol. Aging. 1997; 18: 457-461Google Scholar, 23Sayre L.M. Zelasko D.A. Harris P.L. Perry G. Salomon R.G. Smith M.A. 4-Hydroxynonenal-derived advanced lipid peroxidation end products are increased in Alzheimer’s disease.J. Neurochem. 1997; 68: 2092-2097Google Scholar, 24Markesbery W.R. Carney J.M. Oxidative alterations in Alzheimer’s disease.Brain Pathol. 1999; 9: 133-146Google Scholar) and Parkinson’s (25Morel P. Tallineau C. Pontcharraud R. Piriou A. Huguet F. Effects of 4-hydroxynonenal, a lipid peroxidation product, on dopamine transport and Na+/K+ ATPase in rat striatal synaptosomes.Neurochem. Int. 1998; 33: 531-540Google Scholar) disease. It is highly reactive and covalently binds the NH2 group of lysine residues (26Szweda L.I. Uchida K. Tsai L. Stadtman E.R. Inactivation of glucose-6-phosphate dehydrogenase by 4-hydroxy-2-nonenal. Selective modification of an active-site lysine.J. Biol. Chem. 1993; 268: 3342-3347Google Scholar, 27Nadkarni D.V. Sayre L.M. Structural definition of early lysine and histidine adduction chemistry of 4-hydroxynonenal.Chem. Res. Toxicol. 1995; 8: 284-291Google Scholar, 28Malle E. Ibovnik A. Leis H.J. Kostner G.M. Verhallen P.F. Sattler W. Lysine modification of LDL or lipoprotein(a) by 4-hydroxynonenal or malondialdehyde decreases platelet serotonin secretion without affecting platelet aggregability and eicosanoid formation.Arterioscler. Thromb. Vasc. Biol. 1995; 15: 377-384Google Scholar, 29Selley M.L. Bartlett M.R. Czeti A.L. Ardlie N.G. The role of (E)-4-hydroxy-2-nonenal in platelet activation by low density lipoprotein and iron.Atherosclerosis. 1998; 140: 105-112Google Scholar) to form Michael and Schiff base adducts. It may also react with thiol groups (30Jessup W. Jurgens G. Lang J. Esterbauer H. Dean R.T. Interaction of 4-hydroxynonenal-modified low-density lipoproteins with the fibroblast apolipoprotein B/E J. Scholar, P. Lipid and thiol in isolated rat of E and Biol. Scholar, W.G. H. T. Esterbauer H. of 4-hydroxynonenal in is the main Lipid Res. 1997; Scholar) and Michael adducts in 4-HNE has been described to alter many such as A. M. I. R. S. M. Tsai L. of by Biophys. 1998; Scholar), dehydrogenase B. Stadtman E.R. Szweda L.I. of glucose-6-phosphate dehydrogenase by 4-hydroxy-2-nonenal. of that the Biol. Chem. Scholar), and low density lipoproteins (26Szweda L.I. Uchida K. Tsai L. Stadtman E.R. Inactivation of glucose-6-phosphate dehydrogenase by 4-hydroxy-2-nonenal. Selective modification of an active-site lysine.J. Biol. Chem. 1993; 268: 3342-3347Google Scholar, 27Nadkarni D.V. Sayre L.M. Structural definition of early lysine and histidine adduction chemistry of 4-hydroxynonenal.Chem. Res. Toxicol. 1995; 8: 284-291Google Scholar, 28Malle E. Ibovnik A. Leis H.J. Kostner G.M. Verhallen P.F. Sattler W. Lysine modification of LDL or lipoprotein(a) by 4-hydroxynonenal or malondialdehyde decreases platelet serotonin secretion without affecting platelet aggregability and eicosanoid formation.Arterioscler. Thromb. Vasc. Biol. 1995; 15: 377-384Google Scholar, 29Selley M.L. Bartlett M.R. Czeti A.L. Ardlie N.G. The role of (E)-4-hydroxy-2-nonenal in platelet activation by low density lipoprotein and iron.Atherosclerosis. 1998; 140: 105-112Google Scholar). with 4-HNE also been described for H.J. of adducts of with the aldehydes and in Res. Scholar, M. D. P. E. of a for the of adducts of in Res. Toxicol. 2000; Scholar) and M. P. Lagarde M. of by Radic. Biol. Med. 1998; Scholar). The main compounds with PE Michael and Schiff base the latter of which was partially may with a of PE can adducts with T.J. B. of and two products of modification of in 1999; Scholar) and lysine residues with aldehydes Elevated levels of an aldehyde by are present in human fatty and advanced J. 2000; Scholar). The first of the present study was to 12-HpETE be degraded into putative aldehyde 4-HDDE as from 15-HpETE to 4-HNE, and to that such a is in The of the study was to compare the ability of 4-HNE, and 4-HDDE, which different hydrophobicity, to covalently modify molecular species of species and docosahexaenoyl-containing PEs in diacyl and plasmalogen subclasses from rat chosen because of their biological and and from and from from was from was from a of and in was a of in The was at The was reduced and the was on with as to a of in at was a of of in with of The was to from to and the was for A acid was at and the to to The was and The was reduced and the was on with as to 4-HDDE in with a are in and are to and are of of of and platelets isolated from human to Lagarde M. M. M. A and for platelet from their Res. 1980; 17: Scholar). was at for The was to with acid and at for and the into was with to reduced glutathione B. a for the oxidation of glutathione to the Biophys. Res. Commun. 1969; Scholar) and and with acid as a The of the effect of on human I. of a 56: Scholar), for at with with of for in the presence of was to with and with of ether to The was to The 12-HpETE formation was with an of the lipid by the acid compounds detected by a The lipid which the 12-HpETE, was for at with of containing and to the by Lang J. C. Esterbauer H. of the lipid peroxidation product 4-hydroxynonenal by 1985; Scholar) to 4-hydroxynonenal from The was with of the The was and the by the as 4-HDDE as a was on the the to the was and the aldehyde was with The aldehyde or was with of in for at to the described by Kuijk Kuijk F.J. R.J. of in oxidized low-density lipoprotein by 1995; Scholar). with of with and and by as The to of 4-HDDE, was and with The was and the group was into an with at The was by two aldehydes been synthesized to was on a with a The was with an which was at The was at increased to at by an to at with a with a of The and at and was at and as and from to the and the The was at brain with a of and phospholipids to and P. G. and of phospholipids and from rat 1985; Scholar). the lipid was in and the was a with with and total phospholipids with The was to by and of was to for The different by the as PE was detected by the with in was and PE was by a of PE subclasses by an to the described by and N. of containing to oxidative Radic. Biol. Med. 1999; 26: Scholar) and as PE was a with A of was used, and the was by of the at The of a with two A and B. A was a of containing to and the as A but in different A was from to at was by a of to at was for and the to the conditions and to and was by their fatty acyl by was with of and of in at the to and in was The fatty acid from diacyl-GPE, and and from alkenylacyl-GPE by of and by with a with a was as the at of the and the at and was as and to of molecular species of PE by was with two of 4-HNE, or 4-HDDE in a containing and and of The aldehyde was by in the The was for at The adducts and the PE with a of and by the as Michael and Schiff base adducts from the and by their fatty acyl by as described in in which was used, of 4-HDDE in two from the to of with R. Y. T. A. of from Scholar, K. I. of 1990; of acid Chem. 1985; Scholar) 4-HDDE was by of with K. H. T. of 2000; Scholar) and to 4-HDDE are as synthesized 4-HDDE was as described in and by in the to and at and of and show the for the of the different the of the at is as an The base at to the of the from the molecular and two at and to the and also at to a of from the at and at from the with a of In to 4-HDDE with in biological was and with the The of and show the for the of the different The of the at is in at of of of and and of the group The to the at as well as at from the and with a of and and the 4-HDDE 12-HpETE was to study by iron and C of was into 12-HpETE by platelets with and as We that 12-HpETE-derived aldehyde was by of 12-HpETE containing with iron and C. The aldehyde was by as described in A of the 12-HpETE as the synthesized The was and group into by The to was and with as described to by with the for their aldehydes first as with as described in was for human two at the as those for the The of the first the as that of 4-HDDE, for by that 4-HDDE was abundant in human from than was 4-HNE a in the of as that of a of rat brain PE in a of different molecular species. and by as described in to their fatty acyl was to be and The reactivity of 4-HNE, and 4-HDDE was by their ability to covalently modify or subclasses isolated by Michael and Schiff base adducts measured by as in that the amount of adducts as of was higher than adducts and than adducts with 4-HNE, and adducts and of the The reactivity of the aldehydes, on their hydrophobicity, with 4-HDDE the most and the hydrophobic aldehydes. with the alkenylacyl-GPE subclasses 4-HNE, and 4-HDDE with or The of the adducts and represent and of and the of and adducts represent and we that 4-HDDE, the most hydrophobic aldehyde, was more in adducts with alkenylacyl-GPE than 4-HNE and 4-HHE. to in and and compared to the PE subclasses and to the of the fatty acid at the sn-2 that the fatty acid at the sn-2 aldehydes more for adducts with the group of alkenylacyl-GPE than with that of The amount produced from the was higher than with the the aldehyde The group of alkenylacyl-GPE be more than that of to of adducts with the different of PE adducts adducts adducts adducts ethanolamine diacyl-GPE, 4-HNE, 4-HDDE, are from and represent the of and are compared as adducts adducts adducts adducts in a ethanolamine diacyl-GPE, 4-HNE, 4-HDDE, are from and represent the of and are compared as Also, the reactivity of different aldehydes toward PE in and for of the ability of these aldehydes to covalently modify PE to the of the fatty acid at the sn-2 the PE The amount of the adducts was more with PE at the sn-2 position than with of adducts with the different PE of represent the of in and of the fatty acid at the sn-2 position of PE on the the aldehyde represent the of in and in a of the fatty acid at the sn-2 position of PE on the the aldehyde Lipid peroxidation leads to the formation of fatty aldehydes, such as and (12Esterbauer H. McBrien D.C.H. Slater T.F. Aldehydic Products of Lipid Peroxidation: Free Radicals Lipid Peroxidation and Cancer. Academic Press, London1982: 101-128Google Scholar, 13Poli G. Dianzani M.U. Cheeseman K.H. Slater T.F. Lang J. Esterbauer H. Separation and characterization of the aldehydic products of lipid peroxidation stimulated by carbon tetrachloride or ADP-iron in isolated rat hepatocytes and rat liver microsomal suspensions.Biochem. J. 1985; 227: 629-638Google Scholar). aldehydes are more than hydroperoxides, and are to 4-HNE is of the major products of peroxidation, and many biological It is by the breakdown of fatty acid issued from the peroxidation of n-6 15-HpETE from for the of from the of polyunsaturated fatty Radic. Biol. Med. 1990; 8: Scholar, of oxidation of 1995; Scholar). 15-HpETE is the fatty acid in a of 12(S)-HpETE is produced in cells 12-lipoxygenase platelets M. B. of arachidonic acid in human Scholar), in addition to 12-HpETE by of AA. the of the 15-HpETE we a of to the potential of 12-HpETE to form homologous aldehydes. the 4-HDDE was and was by and 4-HDDE was of because was to into 4-HDDE from and 12-lipoxygenation of AA. a which is to be compared with the of 4-HDDE P. P. S. J. total of of and Scholar, P. S. P. J. total of and Scholar). In the of in the is an for the of 4-HDDE issued from and 12-lipoxygenation of AA. that 12-HpETE from human platelets and with a of C and iron is degraded into aldehyde with the as that for the degradation of 15-HpETE into 4-HNE The of the aldehyde homologous to 4-HNE was by and compared with that of was to the in biological The of and of the issued from the 12-HpETE-derived aldehyde the and the as those of synthesized We conclude that 12-HpETE can be by a which that by and for the of from the of polyunsaturated fatty Radic. Biol. Med. 1990; 8: Scholar) for the degradation of 15-HpETE into 4-HNE. 4-HNE and 4-HDDE detected by in human and that the amount of 4-HNE measured was higher than that of 4-HDDE may be produced in from and/or reactive oxygen 12(S)-HpETE formation is platelets are and the GPx and/or glutathione activities are which to increased 4-HDDE In 4-HNE is to be specific because from peroxidation of n-6 and In the of the present we to the reactivity of 4-HDDE with the of because 4-HNE has been to adducts with M. P. Lagarde M. of by Radic. Biol. Med. 1998; Scholar). Also, issued from n-3 was as a PE subclasses containing or DHA at the sn-2 position investigated. The show that 4-HDDE is more reactive than 4-HNE, which is also more reactive than with PE The was with the alkenylacyl-GPE The with containing that 4-HNE to more adducts than and that 4-HDDE to more adducts than 4-HNE. Moreover, the and alkenylacyl-GPE toward the different aldehydes that ethanolamine plasmalogen are more reactive than the diacyl can be due to a of the group as has been described by and R.W. and 1990; Scholar). the and/or the of alkenylacyl-GPE the ethanolamine and with aldehydes. The higher reactivity of the alkenylacyl-GPEs be in addition to their antioxidant properties to the presence of the vinyl ether alkenylacyl-GPEs may scavenge aldehydes more efficiently and their the of different PE molecular species containing or at the sn-2 position that aldehydes more adducts with PE with is to a than AA. alter the of the in the as has been for lipid R.W. and 1990; Scholar), a of the group to the with a are in with a of the group to the aldehydes show that of adducts be in platelets with such of PE in that may alter the and Moreover, Michael adducts are of M. N. B. C. Lagarde M. from n-6 fatty acid on 67: Scholar). adducts issued from and/or 4-HDDE may the as In 4-HDDE, which is in human be as a of oxidation by The reactivity of the different fatty aldehydes to adducts with PE is by their and is more with alkenylacyl-GPE than with be to the of the in the was by and by a from the which also in of arachidonic acid (20:4n-6) alkenylacyl-glycerophosphoethanolamine diacyl-glycerophosphoethanolamine docosahexaenoic acid (22:6n-3) fatty acid glutathione 4-hydroxydodeca-(2E,6Z)-dienal 4-hydroxy-2E-hexenal 4-hydroxy-2E-nonenal acid ethanolamine reactive oxygen species
No takes yet. Share an insight, caveat, or question.
Bacot et al. (2003) studied this question.
Synapse has enriched one closely related paper. Consider it for comparative context: