Linoleic acid (LA) is an organic compound with the formula HOOC(CH2)7CH=CHCH2CH=CH(CH2)4CH3. Both alkene groups (−CH=CH−) are cis. It is a fatty acid sometimes denoted 18:2 (n−6) or 18:2 cis-9,12. A linoleate is a salt or ester of this acid.
Linoleic acid is a polyunsaturated, omega−6 fatty acid. It is a colorless liquid that is virtually insoluble in water but soluble in many organic solvents. It typically occurs in nature as a triglyceride (ester of glycerin) rather than as a free fatty acid. It is one of two essential fatty acids for humans, who must obtain it through their diet, and the most essential, because the body uses it as a base to make the others.
The word "linoleic" derives from Latin linum 'flax' and oleum 'oil', reflecting the fact that it was first isolated from linseed oil. |
Read full article at Wikipedia
|
InChI=1S/C18H32O2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18(19)20/h6-7,9-10H,2-5,8,11-17H2,1H3,(H,19,20)/b7-6-,10-9- |
OYHQOLUKZRVURQ-HZJYTTRNSA-N |
CCCCC\C=C/C\C=C/CCCCCCCC(O)=O |
|
Carthamus oxyacantha
(NCBI:txid122010)
|
Found in
aerial part
(BTO:0001658).
Crude ethanolic extract of aerial parts
See:
PubMed
|
Daphnia galeata
(NCBI:txid27404)
|
See:
Is the fatty acid composition of Daphnia galeata determined by the fatty acid composition of the ingested diet?Weers P.M.M., Siewertsen K., and Gulati R.D.Freshwater Biology (1997), 38, 731-738
|
Chlamydomonas reinhardtii
(NCBI:txid3055)
|
See:
PubMed
|
Bronsted acid
A molecular entity capable of donating a hydron to an acceptor (Bronsted base).
(via oxoacid )
|
|
algal metabolite
Any eukaryotic metabolite produced during a metabolic reaction in algae including unicellular organisms like chlorella and diatoms to multicellular organisms like giant kelps and brown algae.
Daphnia galeata metabolite
A Daphnia metabolite produced by the species Daphnia galeata.
plant metabolite
Any eukaryotic metabolite produced during a metabolic reaction in plants, the kingdom that include flowering plants, conifers and other gymnosperms.
|
|
View more via ChEBI Ontology
Outgoing
|
linoleic acid
(CHEBI:17351)
has role
Daphnia galeata metabolite
(CHEBI:83038)
linoleic acid
(CHEBI:17351)
has role
algal metabolite
(CHEBI:84735)
linoleic acid
(CHEBI:17351)
has role
plant metabolite
(CHEBI:76924)
linoleic acid
(CHEBI:17351)
is a
ω−6 fatty acid
(CHEBI:36009)
linoleic acid
(CHEBI:17351)
is a
octadecadienoic acid
(CHEBI:25627)
linoleic acid
(CHEBI:17351)
is conjugate acid of
linoleate
(CHEBI:30245)
|
|
Incoming
|
(11S)-11-hydroperoxylinoleic acid
(CHEBI:15657)
has functional parent
linoleic acid
(CHEBI:17351)
(24S)-24-hydroxycholesterol 3-linoleoate
(CHEBI:82875)
has functional parent
linoleic acid
(CHEBI:17351)
(9S),10-epoxy-(10,12Z)-octadecadienoic acid
(CHEBI:143790)
has functional parent
linoleic acid
(CHEBI:17351)
(9Z,12Z)-11-hydroxyoctadecadienoic acid
(CHEBI:137305)
has functional parent
linoleic acid
(CHEBI:17351)
1,1ʼ,2-trilinoleoyl-2ʼ-oleoyl cardiolipin
(CHEBI:84399)
has functional parent
linoleic acid
(CHEBI:17351)
1,1ʼ,2-trilinoleoyl-2ʼ-palmitoyl cardiolipin
(CHEBI:84400)
has functional parent
linoleic acid
(CHEBI:17351)
1,1'-dilinoleoyl-2-oleoyl monolysocardiolipin
(CHEBI:84583)
has functional parent
linoleic acid
(CHEBI:17351)
1,2,2ʼ-trilinoleoyl-,1ʼ-monolysocardiolipin
(CHEBI:84581)
has functional parent
linoleic acid
(CHEBI:17351)
1,2,3-trilinoleoylglycerol
(CHEBI:75844)
has functional parent
linoleic acid
(CHEBI:17351)
1,2-di-(9Z,12Z-octadecadienoyl)-sn-glycero-3-phosphoethanolamine
(CHEBI:84846)
has functional parent
linoleic acid
(CHEBI:17351)
1,2-di-[(9Z,12Z)-octadecadienoyl]-sn-glycero-3-phosphocholine
(CHEBI:42027)
has functional parent
linoleic acid
(CHEBI:17351)
1,2-dilinoleoyl-3-[α-D-galactosyl-(1→6)-β-D-galactosyl]-sn-glycerol
(CHEBI:136796)
has functional parent
linoleic acid
(CHEBI:17351)
1,2-dilinoleoyl-sn-glycero-3-phospho-1D-myo-inositol
(CHEBI:77348)
has functional parent
linoleic acid
(CHEBI:17351)
1,2-dilinoleoyl-sn-glycero-3-phospho-1D-myo-inositol 5-phosphate
(CHEBI:77349)
has functional parent
linoleic acid
(CHEBI:17351)
1,2-dilinoleoyl-sn-glycerol
(CHEBI:77127)
has functional parent
linoleic acid
(CHEBI:17351)
1,2-dioleoyl-3-linoleoyl-sn-glycerol
(CHEBI:77683)
has functional parent
linoleic acid
(CHEBI:17351)
1,3-dilinoleoylglycerol
(CHEBI:75850)
has functional parent
linoleic acid
(CHEBI:17351)
1-(1Z,11Z-octadecadienyl)-2-linoleoyl-sn-glycero-3-phosphoethanolamine
(CHEBI:90486)
has functional parent
linoleic acid
(CHEBI:17351)
1-(1Z-hexadecenyl)-2-(9Z,12Z-octadecadienoyl)-sn-glycero-3-phosphocholine
(CHEBI:84557)
has functional parent
linoleic acid
(CHEBI:17351)
1-(1Z-hexadecenyl)-2-linoleoyl-sn-glycero-3-phosphoethanolamine
(CHEBI:84532)
has functional parent
linoleic acid
(CHEBI:17351)
1-(1Z-octadecenyl)-2-(9Z,12Z-octadecadienoyl)-sn-glycero-3-phosphocholine
(CHEBI:84555)
has functional parent
linoleic acid
(CHEBI:17351)
1-(1Z-octadecenyl)-2-linoleoyl-sn-glycero-3-phosphoethanolamine
(CHEBI:90483)
has functional parent
linoleic acid
(CHEBI:17351)
1-O-linoleoyl-N-acetylsphingosine
(CHEBI:76086)
has functional parent
linoleic acid
(CHEBI:17351)
1-[(10Z,13Z,16Z)-docosatrienoyl]-2-linoleoyl-sn-glycero-3-phospho-1D-myo-inositol
(CHEBI:89249)
has functional parent
linoleic acid
(CHEBI:17351)
1-[(13Z,16Z)-docosadienoyl]-2-linoleoyl-sn-glycero-3-phospho-1D-myo-inositol
(CHEBI:89245)
has functional parent
linoleic acid
(CHEBI:17351)
1-[(5Z,8Z,11Z,14Z)-eicosatetraenoyl]-2-[(9Z,12Z)-octadecadienoyl]-sn-glycero-3-phosphocholine
(CHEBI:86184)
has functional parent
linoleic acid
(CHEBI:17351)
1-[(9Z,12Z)-octadecadienoyl]-2-[(5Z,8Z,11Z,14Z)-icosatetraenoyl]-sn-glycero-3-phosphocholine
(CHEBI:84563)
has functional parent
linoleic acid
(CHEBI:17351)
1-[(9Z,12Z)-octadecadienoyl]-2-hexadecanoyl-sn-glycero-3-phosphocholine
(CHEBI:86099)
has functional parent
linoleic acid
(CHEBI:17351)
1-[(9Z,12Z)-octadecadienoyl]-2-icosanoyl-sn-glycerol
(CHEBI:86985)
has functional parent
linoleic acid
(CHEBI:17351)
1-[(9Z,12Z)-octadecadienoyl]-2-octadecanoyl-sn-glycero-3-phosphocholine
(CHEBI:86112)
has functional parent
linoleic acid
(CHEBI:17351)
1-[(9Z,12Z)-octadecadienoyl]-2-octadecanoyl-sn-glycerol
(CHEBI:86337)
has functional parent
linoleic acid
(CHEBI:17351)
1-acyl-2-linoleoyl-sn-glycero-3-phosphate
(CHEBI:75110)
has functional parent
linoleic acid
(CHEBI:17351)
1-acyl-2-linoleoyl-sn-glycero-3-phosphocholine betaine
(CHEBI:60000)
has functional parent
linoleic acid
(CHEBI:17351)
1-acyl-2-linoleoyl-sn-glycero-3-phosphoethanolamine zwitterion
(CHEBI:75069)
has functional parent
linoleic acid
(CHEBI:17351)
1-eicosyl-2-linolenyl-sn-glycero-3-phosphoethanolamine
(CHEBI:84535)
has functional parent
linoleic acid
(CHEBI:17351)
1-heptadecanoyl-2-(9Z,12Z-octadecadienoyl)-sn-glycero-3-phosphocholine
(CHEBI:84566)
has functional parent
linoleic acid
(CHEBI:17351)
1-hexadecanoyl-2-(9Z,12Z-octadecadienoyl)-sn-glycero-3-phosphoethanolamine
(CHEBI:73121)
has functional parent
linoleic acid
(CHEBI:17351)
1-hexadecyl-2-[(9Z,12Z)-octadecadienoyl]-sn-glycero-3-phosphocholine
(CHEBI:86231)
has functional parent
linoleic acid
(CHEBI:17351)
1-icosyl-2-[(9Z,12Z)-octadecadienoyl]-sn-glycero-3-phosphocholine
(CHEBI:136381)
has functional parent
linoleic acid
(CHEBI:17351)
1-linolenyl-2-linoleyl-PAP
(CHEBI:53755)
has functional parent
linoleic acid
(CHEBI:17351)
1-linoleoyl-2-oleoyl-sn-glycero-3-phosphate
(CHEBI:74830)
has functional parent
linoleic acid
(CHEBI:17351)
1-linoleoyl-2-oleoylglycerol
(CHEBI:75614)
has functional parent
linoleic acid
(CHEBI:17351)
1-linoleoyl-sn-glycero-3-phospho-D-myo-inositol
(CHEBI:133077)
has functional parent
linoleic acid
(CHEBI:17351)
1-linoleoyl-sn-glycero-3-phosphocholine
(CHEBI:28733)
has functional parent
linoleic acid
(CHEBI:17351)
1-linoleoyl-sn-glycero-3-phosphoethanolamine
(CHEBI:83058)
has functional parent
linoleic acid
(CHEBI:17351)
1-linoleoylglycerone 3-phosphate
(CHEBI:78173)
has functional parent
linoleic acid
(CHEBI:17351)
1-monolinolein
(CHEBI:75568)
has functional parent
linoleic acid
(CHEBI:17351)
1-myristoyl-2-linoleoyl-sn-glycerol
(CHEBI:84392)
has functional parent
linoleic acid
(CHEBI:17351)
1-octadecanoyl-2-[(9Z,12Z)-octadecadienoyl]-sn-glycero-3-phosphocholine
(CHEBI:84822)
has functional parent
linoleic acid
(CHEBI:17351)
1-oleoyl-2,3-di-linoleoyl-sn-glycerol
(CHEBI:84458)
has functional parent
linoleic acid
(CHEBI:17351)
1-oleoyl-2-linoleoyl-sn-glycero-3-phosphate
(CHEBI:74849)
has functional parent
linoleic acid
(CHEBI:17351)
1-oleoyl-2-linoleoyl-sn-glycero-3-phospho-L-serine
(CHEBI:75096)
has functional parent
linoleic acid
(CHEBI:17351)
1-oleoyl-2-linoleoyl-sn-glycerol
(CHEBI:75450)
has functional parent
linoleic acid
(CHEBI:17351)
1-oleoyl-2-linoleyl-sn-glycero-3-phosphoethanolamine
(CHEBI:84543)
has functional parent
linoleic acid
(CHEBI:17351)
1-oleoyl-3-linoleoylglycerol
(CHEBI:133484)
has functional parent
linoleic acid
(CHEBI:17351)
1-oleyl-2-linoleyl-PAP
(CHEBI:53752)
has functional parent
linoleic acid
(CHEBI:17351)
1-palmitoleoyl-2-linoleoyl-sn-glycero-3-phosphocholine
(CHEBI:84567)
has functional parent
linoleic acid
(CHEBI:17351)
1-palmitoleoyl-2-linoleoyl-sn-glycerol
(CHEBI:84419)
has functional parent
linoleic acid
(CHEBI:17351)
1-palmitoyl-2-linoleoyl-sn-glycerol
(CHEBI:82927)
has functional parent
linoleic acid
(CHEBI:17351)
1-palmitoyl-3-linoleoylglycerol
(CHEBI:133640)
has functional parent
linoleic acid
(CHEBI:17351)
1-palmityl-2-acetyl-3-linoleoyl-sn-glycerol
(CHEBI:77676)
has functional parent
linoleic acid
(CHEBI:17351)
1-pentadecanoyl-2-linoleoyl-sn-glycero-3-phosphocholine
(CHEBI:133617)
has functional parent
linoleic acid
(CHEBI:17351)
1-stearoyl-2-linoleoyl-sn-glycero-3-phospho-1D-myo-inositol
(CHEBI:77343)
has functional parent
linoleic acid
(CHEBI:17351)
1-stearoyl-2-linoleoyl-sn-glycero-3-phospho-1D-myo-inositol 5-phosphate
(CHEBI:77344)
has functional parent
linoleic acid
(CHEBI:17351)
1-stearoyl-2-linoleoyl-sn-glycero-3-phospho-L-serine
(CHEBI:84513)
has functional parent
linoleic acid
(CHEBI:17351)
1-stearoyl-2-linoleoyl-sn-glycero-3-phosphoethanolamine
(CHEBI:133600)
has functional parent
linoleic acid
(CHEBI:17351)
1-stearoyl-2-linoleoyl-sn-glycerol
(CHEBI:77097)
has functional parent
linoleic acid
(CHEBI:17351)
1-tetradecanoyl-2-[(9Z,12Z)-octadecadienoyl]-sn-glycero-3-phosphocholine
(CHEBI:86094)
has functional parent
linoleic acid
(CHEBI:17351)
12,13-epoxy-18-hydroxy-(9Z)-octadecenoic acid
(CHEBI:138270)
has functional parent
linoleic acid
(CHEBI:17351)
13-hydroperoxylinoleic acid
(CHEBI:50097)
has functional parent
linoleic acid
(CHEBI:17351)
18-hydroxylinoleic acid
(CHEBI:132472)
has functional parent
linoleic acid
(CHEBI:17351)
2,3-dilinoleoyl-sn-glycerol
(CHEBI:75854)
has functional parent
linoleic acid
(CHEBI:17351)
2-hydroxylinoleic acid
(CHEBI:136927)
has functional parent
linoleic acid
(CHEBI:17351)
2-linoleoyl-sn-glycero-3-phosphocholine
(CHEBI:76084)
has functional parent
linoleic acid
(CHEBI:17351)
2-linoleoyl-sn-glycero-3-phosphoethanolamine
(CHEBI:76233)
has functional parent
linoleic acid
(CHEBI:17351)
2-linoleoyl-sn-glycero-3-phosphoethanolamine zwitterion
(CHEBI:76090)
has functional parent
linoleic acid
(CHEBI:17351)
2-linoleoylglycerol
(CHEBI:75457)
has functional parent
linoleic acid
(CHEBI:17351)
5(S),8(R)-DiHODE
(CHEBI:63216)
has functional parent
linoleic acid
(CHEBI:17351)
7(S),8(S)-DiHODE
(CHEBI:15658)
has functional parent
linoleic acid
(CHEBI:17351)
7-demethoxyegonol-9(Z),12(Z)linoleate
(CHEBI:69547)
has functional parent
linoleic acid
(CHEBI:17351)
8(R)-HPODE
(CHEBI:34485)
has functional parent
linoleic acid
(CHEBI:17351)
9,10-epoxy-18-hydroxy-(12Z)-octadecenoic acid
(CHEBI:138265)
has functional parent
linoleic acid
(CHEBI:17351)
all-trans-retinyl linoleate
(CHEBI:70762)
has functional parent
linoleic acid
(CHEBI:17351)
N,1-dipalmitoyl-2-linoleoyl-sn-glycero-3-phosphoethanolamine
(CHEBI:85806)
has functional parent
linoleic acid
(CHEBI:17351)
N-butyryl-1-palmitoyl-2-linoleoyl-sn-glycero-3-phosphoethanolamine
(CHEBI:85799)
has functional parent
linoleic acid
(CHEBI:17351)
N-caproyl-1-palmitoyl-2-linoleoyl-sn-glycero-3-phosphoethanolamine
(CHEBI:85798)
has functional parent
linoleic acid
(CHEBI:17351)
N-capryl-1-palmitoyl-2-linoleoyl-sn-glycero-3-phosphoethanolamine
(CHEBI:85796)
has functional parent
linoleic acid
(CHEBI:17351)
N-capryloyl-1-palmitoyl-2-linoleoyl-sn-glycero-3-phosphoethanolamine
(CHEBI:85797)
has functional parent
linoleic acid
(CHEBI:17351)
O-linoleyl-L-carnitine
(CHEBI:84098)
has functional parent
linoleic acid
(CHEBI:17351)
CDP-1,2-dilinoleoyl-sn-glycerol
(CHEBI:85848)
has functional parent
linoleic acid
(CHEBI:17351)
CDP-1-stearoyl-2-linoleoyl-sn-glycerol
(CHEBI:85838)
has functional parent
linoleic acid
(CHEBI:17351)
cholesteryl linoleate
(CHEBI:41509)
has functional parent
linoleic acid
(CHEBI:17351)
dilinoleoylglycerol
(CHEBI:138658)
has functional parent
linoleic acid
(CHEBI:17351)
egonol-9(Z),12(Z)linoleate
(CHEBI:69546)
has functional parent
linoleic acid
(CHEBI:17351)
ethyl linoleate
(CHEBI:31572)
has functional parent
linoleic acid
(CHEBI:17351)
HPODE
(CHEBI:36329)
has functional parent
linoleic acid
(CHEBI:17351)
laetisaric acid
(CHEBI:28932)
has functional parent
linoleic acid
(CHEBI:17351)
linoleamide
(CHEBI:82984)
has functional parent
linoleic acid
(CHEBI:17351)
linoleic acid hydroperoxide
(CHEBI:78013)
has functional parent
linoleic acid
(CHEBI:17351)
linoleoyl bioconjugate
(CHEBI:76186)
has functional parent
linoleic acid
(CHEBI:17351)
linoleoyl ethanolamide
(CHEBI:64032)
has functional parent
linoleic acid
(CHEBI:17351)
linoleoyl-sn-glycero-3-phosphocholine
(CHEBI:140444)
has functional parent
linoleic acid
(CHEBI:17351)
linoleoyl-containing glycerolipid
(CHEBI:88351)
has functional parent
linoleic acid
(CHEBI:17351)
linoleylanilide
(CHEBI:53722)
has functional parent
linoleic acid
(CHEBI:17351)
methyl linoleate
(CHEBI:69080)
has functional parent
linoleic acid
(CHEBI:17351)
propyl linoleate
(CHEBI:91035)
has functional parent
linoleic acid
(CHEBI:17351)
tetralinoleoyl cardiolipin
(CHEBI:84398)
has functional parent
linoleic acid
(CHEBI:17351)
trilinoleoyl 2-monolysocardiolipin
(CHEBI:84302)
has functional parent
linoleic acid
(CHEBI:17351)
corn oil
(CHEBI:195250)
has part
linoleic acid
(CHEBI:17351)
soybean oil
(CHEBI:166975)
has part
linoleic acid
(CHEBI:17351)
linoleate
(CHEBI:30245)
is conjugate base of
linoleic acid
(CHEBI:17351)
linoleoyl group
(CHEBI:32386)
is substituent group from
linoleic acid
(CHEBI:17351)
|
(9Z,12Z)-octadeca-9,12-dienoic acid
|
(9Z,12Z)-Octadecadienoic acid
|
KEGG COMPOUND
|
(Z,Z)-9,12-octadecadienoic acid
|
NIST Chemistry WebBook
|
9-cis,12-cis-Octadecadienoic acid
|
KEGG COMPOUND
|
9Z,12Z-octadecadienoic acid
|
LIPID MAPS
|
acide cis-linoléique
|
ChEBI
|
acide linoléique
|
ChEBI
|
ácido linoleico
|
ChEBI
|
all-cis-9,12-octadecadienoic acid
|
ChEBI
|
C18:2 9c, 12c ω6 todos cis-9,12-octadienoico
|
ChEBI
|
C18:2, n-6,9 all-cis
|
ChEBI
|
cis,cis-9,12-octadecadienoic acid
|
ChEBI
|
cis,cis-linoleic acid
|
ChEBI
|
cis,cis-linoleic acid
|
NIST Chemistry WebBook
|
cis-Δ9,12-octadecadienoic acid
|
ChemIDplus
|
LA
|
ChEBI
|
Linoleic acid
|
KEGG COMPOUND
|
LINOLEIC ACID
|
PDBeChem
|
linolic acid
|
ChEBI
|
1727101
|
Reaxys Registry Number
|
Reaxys
|
57557
|
Gmelin Registry Number
|
Gmelin
|
60-33-3
|
CAS Registry Number
|
KEGG COMPOUND
|
60-33-3
|
CAS Registry Number
|
NIST Chemistry WebBook
|
60-33-3
|
CAS Registry Number
|
ChemIDplus
|
Choque B, Catheline D, Rioux V, Legrand P (2014) Linoleic acid: between doubts and certainties. Biochimie 96, 14-21 [PubMed:23900039] [show Abstract] Linoleic acid is the most abundant polyunsaturated fatty acid in human nutrition and represents about 14 g per day in the US diet. Following the discovery of its essential functions in animals and humans in the early 1920's, studies are currently questioning the real requirement of linoleic acid. It seems now overestimated and creates controversy: how much linoleic acid should be consumed in a healthy diet? Beyond the necessity to redefine the dietary requirement of linoleic acid, many questions concerning the consequences of its excessive consumption on human health arise. Linoleic acid is a direct precursor of the bioactive oxidized linoleic acid metabolites. It is also a precursor of arachidonic acid, which produces pro-inflammatory eicosanoids and endocannabinoids. A majority of the studies on linoleic acid and its derivatives show a direct/indirect link with inflammation and metabolic diseases. Many authors claim that a high linoleic acid intake may promote inflammation in humans. This review tries to (i) highlight the importance of reconsidering the actual requirement of linoleic acid (ii) point out the lack of knowledge between dietary levels of linoleic acid and the molecular mechanisms explaining its physiological roles (iii) demonstrate the relevance of carrying out further human studies on the single variable linoleic acid. | Alvheim AR, Torstensen BE, Lin YH, Lillefosse HH, Lock EJ, Madsen L, Frøyland L, Hibbeln JR, Malde MK (2014) Dietary linoleic acid elevates the endocannabinoids 2-AG and anandamide and promotes weight gain in mice fed a low fat diet. Lipids 49, 59-69 [PubMed:24081493] [show Abstract] Dietary intake of linoleic acid (LNA, 18:2n-6) has increased dramatically during the 20th century and is associated with greater prevalence of obesity. The endocannabinoid system is involved in regulation of energy balance and a sustained hyperactivity of the endocannabinoid system may contribute to obesity. Arachidonic acid (ARA, 20:4n-6) is the precursor for 2-AG and anandamide (AEA), and we sought to determine if low fat diets (LFD) could be made obesogenic by increasing the endocannabinoid precursor pool of ARA, causing excessive endocannabinoid signaling leading to weight gain and a metabolic profile associated with obesity. Mice (C57BL/6j, 6 weeks of age) were fed 1 en% LNA and 8 en% LNA in low fat (12.5 en%) and medium fat diets (MFD, 35 en%) for 16 weeks. We found that increasing dietary LNA from 1 to 8 en% in LFD and MFD significantly increased ARA in phospholipids (ARA-PL), elevated 2-AG and AEA in liver, elevated plasma leptin, and resulted in larger adipocytes and more macrophage infiltration in adipose tissue. In LFD, dietary LNA of 8 en% increased feed efficiency and caused greater weight gain than in an isocaloric reduction to 1 en% LNA. Increasing dietary LNA from 1 to 8 en% elevates liver endocannabinoid levels and increases the risk of developing obesity. Thus a high dietary content of LNA (8 en%) increases the adipogenic properties of a low fat diet. | Nomura T, Horikawa M, Shimamura S, Hashimoto T, Sakamoto K (2010) Fat accumulation in Caenorhabditis elegans is mediated by SREBP homolog SBP-1. Genes & nutrition 5, 17-27 [PubMed:19936816] [show Abstract] Research into the metabolism of fats may reveal potential targets for developing pharmaceutical approaches to obesity and related disorders. Such research may be limited, however, by the cost and time involved in using mammalian subjects or developing suitable cell lines. To determine whether invertebrates could be used to carry out such research more efficiently, we investigated the ability of Caenorhabditis elegans (C. elegans) to accumulate body fat following the consumption of excess calories and the mechanisms it uses to metabolize fat. C. elegans worms were grown on media containing various sugars and monitored for changes in body fat and expression of sbp-1, a homolog of the mammalian transcription factor SREBP-1c, which facilitates fat storage in mammals. The fat content increased markedly in worms exposed to glucose. In situ analysis of gene expression in transgenic worms carrying the GFP-labeled promoter region of sbp-1 revealed that sbp-1 mRNA was strongly expressed in the intestine. An sbp-1 knockdown caused a reduction in body size, fat storage, and egg-laying activity. RT-PCR analysis revealed a considerable decrease in the expression of fatty acid synthetic genes (including elo-2, fat-2, and fat-5) and a considerable increase of starvation-inducible gene acs-2. Normal egg-laying activity and acs-2 expression were restored on exposure to a polyunsaturated fatty acid. These findings suggest that SBP-1 and SREBP regulate the amount and composition of fat and response to starvation in a similar manner. Thus, C. elegans may be an appropriate subject for studying the metabolism of fats. | IBD in EPIC Study Investigators, Tjonneland A, Overvad K, Bergmann MM, Nagel G, Linseisen J, Hallmans G, Palmqvist R, Sjodin H, Hagglund G, Berglund G, Lindgren S, Grip O, Palli D, Day NE, Khaw KT, Bingham S, Riboli E, Kennedy H, Hart A (2009) Linoleic acid, a dietary n-6 polyunsaturated fatty acid, and the aetiology of ulcerative colitis: a nested case-control study within a European prospective cohort study. Gut 58, 1606-1611 [PubMed:19628674] [show Abstract]
ObjectiveDietary linoleic acid, an n-6 polyunsaturated fatty acid, is metabolised to arachidonic acid, a component of colonocyte membranes. Metabolites of arachidonic acid have pro-inflammatory properties and are increased in the mucosa of patients with ulcerative colitis. The aim of this investigation was to conduct the first prospective cohort study investigating if a high dietary intake of linoleic acid increases the risk of developing incident ulcerative colitis.Design and settingDietary data from food frequency questionnaires were available for 203 193 men and women aged 30-74 years, resident in the UK, Sweden, Denmark, Germany or Italy and participating in a prospective cohort study, the European Prospective Investigation into Cancer and Nutrition (EPIC). These participants were followed up for the diagnosis of ulcerative colitis. Each case was matched with four controls and the risk of disease calculated by quartile of intake of linoleic acid adjusted for gender, age, smoking, total energy intake and centre.ResultsA total of 126 participants developed ulcerative colitis (47% women) after a median follow-up of 4.0 years (range, 1.7-11.3 years). The highest quartile of intake of linoleic acid was associated with an increased risk of ulcerative colitis (odds ratio (OR) = 2.49, 95% confidence interval (CI) = 1.23 to 5.07, p = 0.01) with a significant trend across quartiles (OR = 1.32 per quartile increase, 95% CI = 1.04 to 1.66, p = 0.02 for trend).ConclusionsThe data support a role for dietary linoleic acid in the aetiology of ulcerative colitis. An estimated 30% of cases could be attributed to having dietary intakes higher than the lowest quartile of linoleic acid intake. | Whelan J (2008) The health implications of changing linoleic acid intakes. Prostaglandins, leukotrienes, and essential fatty acids 79, 165-167 [PubMed:18990554] [show Abstract] Linoleic acid is the most prominent polyunsaturated fatty acid (PUFA) in the Western diet. It is virtually found in every food we eat and is the predominant PUFA in land-based meats, dairy, vegetables, vegetable oils, cereals, fruits, nuts, legumes, seeds and breads. Because linoleic acid is the metabolic precursor of arachidonic acid and bioactive eicosanoids derived from arachidonic acid, there is concern that dietary linoleic acid could augment tissue arachidonic acid content, eicosanoid formation and subsequently enhance the risk of and/or exacerbate conditions associated with acute and chronic diseases (i.e., cancers, cardiovascular disease, inflammation, neurological disorders, etc.). The following series of papers examines the impact of modifying dietary levels of linoleic acid on health outcomes. The authors were asked to start with current intakes of linoleic acid (adults) and determine if health outcomes would change if linoleic acid intake increased or decreased. The authors addressed changes in tissue arachidonic acid content and eicosanoid formation, cardiovascular disease, inflammation, and psychiatric disorders. | Haddada FM, Manaï H, Oueslati I, Daoud D, Sánchez J, Osorio E, Zarrouk M (2007) Fatty acid, triacylglycerol, and phytosterol composition in six Tunisian olive varieties. Journal of agricultural and food chemistry 55, 10941-10946 [PubMed:18044828] [show Abstract] The physicochemical and stability properties as well as the fatty acid, triacylglycerol, sterol, and triterpenic dialcohol compositions of Tunisian olive oil varieties were analyzed. On the basis of our results, we classified all of the monovarietal oils into the extra virgin category. Oleic and linoleic acids were the most useful fatty acids to discriminate three cultivars, Neb Jmel, Chétoui, and Ain Jarboua, from the others. Of the six monovarietal virgin olive oils analyzed, the main triacylglycerols were OOO, POO, PLO plus SLL, and OLO, which was expected given the high oleic acid and low linoleic and linolenic acids content observed in total fatty acids. In total, these accounted for more than 80% of the total HPLC chromatogram peak area. The main sterols found were beta-sitosterol, Delta5-avenasterol, and campesterol. The statistical analysis showed significant differences between oil samples, and the obtained results showed a great variability in the oil composition between cultivars, which is influenced exclusively by genetic factors. | Pérez-Matute P, Martínez JA, Marti A, Moreno-Aliaga MJ (2007) Linoleic acid decreases leptin and adiponectin secretion from primary rat adipocytes in the presence of insulin. Lipids 42, 913-920 [PubMed:17647039] [show Abstract] Obesity rates have dramatically increased over the last few decades and, at the same time, major changes in the type of fatty acid intake have occurred. Linoleic acid, an n-6 polyunsaturated fatty acid, is an essential fatty acid occurring in high amounts in several western diets. A potential role of this fatty acid on obesity has been suggested. Controversial effects of linoleic acid on insulin sensitivity have also been reported. Thus, the aim of this study was to examine the direct effects of linoleic acid on leptin and adiponectin production, two adipokines known to influence weight gain and insulin sensitivity. Because insulin-stimulated glucose metabolism is an important regulator of leptin production, the effects of linoleic acid on adipocyte metabolism were also examined. For this purpose, isolated rat adipocytes were incubated with linoleic acid (1-200 microM) in the absence or presence of insulin. Linoleic acid (1-200 microM) significantly decreased insulin-stimulated leptin secretion and expression (P < 0.05), however, no changes in basal leptin production were observed. Linoleic acid also induced a significant decrease (approximately 20%) in adiponectin secretion (P < 0.05), but only in the presence of insulin and at the highest concentration tested (200 microM). This fatty acid did not modify either glucose uptake or lactate production and the percentage of glucose metabolized to lactate was not changed either. Together, these results suggest that linoleic acid seems to interfere with other insulin signalling pathway different from those controlling glucose uptake and metabolism, but involved in the regulation of leptin and adiponectin production. | Feng DD, Luo Z, Roh SG, Hernandez M, Tawadros N, Keating DJ, Chen C (2006) Reduction in voltage-gated K+ currents in primary cultured rat pancreatic beta-cells by linoleic acids. Endocrinology 147, 674-682 [PubMed:16254037] [show Abstract] Free fatty acids (FFAs), in addition to glucose, have been shown to stimulate insulin release through the G protein-coupled receptor (GPCR)40 receptor in pancreatic beta-cells. Intracellular free calcium concentration ([Ca(2+)](i)) in beta-cells is elevated by FFAs, although the mechanism underlying the [Ca(2+)](i) increase is still unknown. In this study, we investigated the action of linoleic acid on voltage-gated K(+) currents. Nystatin-perforated recordings were performed on identified rat beta-cells. In the presence of nifedipine, tetrodotoxin, and tolbutamide, voltage-gated K(+) currents were observed. The transient current represents less than 5%, whereas the delayed rectifier current comprises more than 95%, of the total K(+) currents. A long-chain unsaturated FFA, linoleic acid (10 microm), reversibly decreased the amplitude of K(+) currents (to less than 10%). This reduction was abolished by the cAMP/protein kinase A system inhibitors H89 (1 microm) and Rp-cAMP (10 microm) but was not affected by protein kinase C inhibitor. In addition, forskolin and 8'-bromo-cAMP induced a similar reduction in the K(+) current as that evoked by linoleic acid. Insulin secretion and cAMP accumulation in beta-cells were also increased by linoleic acid. Methyl linoleate, which has a similar structure to linoleic acid but no binding affinity to GPR40, did not change K(+) currents. Treatment of cultured cells with GPR40-specific small interfering RNA significantly reduced the decrease in K(+) current induced by linoleic acid, whereas the cAMP-induced reduction of K(+) current was not affected. We conclude that linoleic acid reduces the voltage-gated K(+) current in rat beta-cells through GPR40 and the cAMP-protein kinase A system, leading to an increase in [Ca(2+)](i) and insulin secretion. | Hennig B, Lei W, Arzuaga X, Ghosh DD, Saraswathi V, Toborek M (2006) Linoleic acid induces proinflammatory events in vascular endothelial cells via activation of PI3K/Akt and ERK1/2 signaling. The Journal of nutritional biochemistry 17, 766-772 [PubMed:16563718] [show Abstract] Linoleic acid (18:2n-6), is a major unsaturated fatty acid in the American diet. Linoleic acid is considered to be atherogenic because of its pro-oxidative and proinflammatory properties. There is substantial evidence that linoleic acid (LA) can activate vascular endothelial cells and contribute to an inflammatory response. To explore the mechanisms of LA-induced proinflammatory signaling pathways, the present study addresses the role of the phosphatidylinositol 3-kinase/amino kinase terminal (PI3K/Akt), extracellular signal regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK) pathways during vascular endothelial cell activation. After a 3- to 6-h exposure, LA significantly activated both Akt and ERK in endothelial cells, as assessed by western blot and immunofluorescence. In contrast, LA activated p38 MAPK already at 10 min, suggesting that p38 MAPK signaling occurred upstream of the ERK1/2 pathway. Furthermore, inhibition of ERK activity by PD98059 and PI3K/Akt activity by LY294002 or wortmannin significantly reduced the LA-induced activation of nuclear factor kappa B (NF-kappaB). These results suggest a contribution of both the ERK1/2 and PI3K/Akt pathways to the effect of LA on NF-kappaB-dependent transcription. Indeed, LA-mediated gene expression of the vascular cell adhesion molecule 1 was suppressed by PD98059, wortmannin and LY294002. These data indicate that both PI3K/Akt- and ERK1/2-mediated proinflammatory signaling events are critical in LA-induced endothelial cell activation and vascular inflammation. | Tritt KL, O'Bara CJ, Wells MJ (2005) Chemometric discrimination among wild and cultured age-0 largemouth bass, black crappies, and white crappies based on fatty acid composition. Journal of agricultural and food chemistry 53, 5304-5312 [PubMed:15969511] [show Abstract] The potential to distinguish juvenile wild from cultured fishes and to discriminate among juvenile fishes by species based on fatty acid composition was demonstrated. Statistical approaches to data evaluation included analysis of variance, correlation analysis, principal component analysis (PCA), and quadratic discriminant analysis (QDA). Differences were determined between wild and cultured fishes both within and between species and between hatcheries. Fatty acid compositions were compared among individual (not composited) specimens of wild and cultured, age-0, freshwater species: largemouth bass Micropterus salmoides, black crappies Pomoxis nigromaculatus, white crappies P. annularis, and black-nose crappies. Four fatty acids were investigated: linoleic acid (18:2n-6), linolenic acid (18:3n-3), arachidonic acid (20:4n-6), and docosahexaenoic acid (22:6n-3). Linoleic acid was the primary fatty acid used to differentiate juvenile wild from cultured fishes. Concentrations of linoleic acid were significantly different (p < 0.05) in cultured largemouth bass and black crappies from the wild counterparts. Linolenic acid concentrations were not significantly different (p < 0.05) between wild and cultured largemouth bass but were significantly different between wild and cultured black crappies. Wild largemouth bass contained higher concentrations of arachidonic acid than the cultured bass, and concentrations of docosahexaenoic acid were twice as high in wild black crappies than cultured black crappies. On the basis of four signature fatty acids, 90 of 91 juvenile fishes were correctly classified as wild or cultured; 32 of 37 wild juvenile fishes originating from the same reservoir were differentiated by species. Data from the training set were used to classify a test set of fishes as to species, source, or origin with 100% accuracy. | Cheng Z, Elmes M, Kirkup SE, Chin EC, Abayasekara DR, Wathes DC (2005) The effect of a diet supplemented with the n-6 polyunsaturated fatty acid linoleic acid on prostaglandin production in early- and late-pregnant ewes. The Journal of endocrinology 184, 165-178 [PubMed:15642793] [show Abstract] Polyunsaturated fatty acids derived from the diet are incorporated into cell membranes where they act as precursors for prostaglandin (PG) synthesis. Linoleic acid (LA; 18:2 n-6) is a major constituent of plant oils and its consumption in Westernized populations is increasing. This study investigated the influence of LA on PG production by the uterus and placenta. Pregnant ewes were fed a control or an LA-enriched diet. Oxytocin (OT) was injected on day 45 (early) or day 133 (late) of gestation to measure the release of 13,14-dihydro-15-keto PGF(2alpha) (PGFM). Ewes were killed on day 46 or day 138 for collection of uterine intercaruncular endometrium and fetal allantochorion. Basal and stimulated PG release from explant cultures was assessed before and after in vitro treatment with OT, lipopolysaccharide (LPS), dexamethasone (DEX) or calcium ionophore (CaI). Expression of cyclooxygenase (COX)-1 and COX-2 was determined by Western blot in endometrium of late-gestation ewes. Circulating PGFM levels in vivo did not differ according to diet but there were highly significant differences in the release of PGs in vitro. Basal production of PGF(2alpha)and PGE(2) by the endometrium and of PGE(2) by the allantochorion were all higher in tissues from LA-supplemented ewes. Endometrial tissues produced more PG following OT and CaI treatment, whereas DEX inhibited production of both PGs at both stages of gestation. In allantochorion collected at day 46 LPS did not significantly alter PGE(2) release and DEX increased output, whereas at day 138 LPS was stimulatory but DEX was inhibitory. These data show that a high-LA diet can significantly increase the ability of both endometrium and placental tissues to produce PGs in vitro. This effect of diet may only become apparent after a sustained period of PG release, so was not seen following the brief pulse caused by OT treatment in vivo. As COX protein levels were unaltered, the main influence was likely to be via conversion of LA to arachidonic acid, providing an increased supply of precursor. These results support previous studies which suggest that alterations in dietary polyunsaturated fatty acids may influence the time of labour. | Namazi MR (2004) The beneficial and detrimental effects of linoleic acid on autoimmune disorders. Autoimmunity 37, 73-75 [PubMed:15115315] [show Abstract] Type 1, or cellular, immune response is characterized by overproduction of IL-1, IL-2, IFN-gamma and TNF-alpha and is the underlying immune mechanism of some autoimmune disorders such as psoriasis, alopecia areata, rheumatoid arthritis, Crohn's disease, multiple sclerosis, insulin-dependent diabetes mellitus and experimental autoimmune uveitis. Type 2 immune response is seen in allergic and antibody-mediated autoimmune diseases and is characterized by IL-4, IL-6 and IL-10 overproduction. Linoleic acid is a precursor of prostaglandin E2 (PGE2) and its intake results in tissue production of PGE2, especially in the absence of other polyunsaturated fatty acids (PUFAS) which inhibit this conversion. PGE2 decreases the production of IL-1, IL-2, IFN-gamma and TNF-alpha and proliferation of TH1 cells and increases the production of IL-4, leading to suppression of the type 1 immune response. Taken together, linoleic acid, the major PUFA of maize oil, could have therapeutic efficacy against cellular autoimmune disorders. On the other hand, excessive intake of linoleic acid may aggravate type 2 autoimmune disorders. | Saraswathi V, Wu G, Toborek M, Hennig B (2004) Linoleic acid-induced endothelial activation: role of calcium and peroxynitrite signaling. Journal of lipid research 45, 794-804 [PubMed:14993245] [show Abstract] Hypertriglyceridemia, an important risk factor of atherosclerosis, is associated with increased circulating free fatty acids. Research to date indicates that linoleic acid (LA), the major fatty acid in the American diet, may be atherogenic by activating vascular endothelial cells. However, the exact signaling mechanisms involved in LA-mediated proinflammatory events in endothelial cells still remain unclear. We previously reported increased superoxide formation after LA exposure in endothelial cells. The objective of the present investigation is to determine the role of calcium and peroxynitrite in mediating the proinflammatory effect of LA in vascular endothelial cells. LA exposure increased intracellular calcium, nitric oxide, and tetrahydrodiopterin levels as well as the expression of E-selectin. Inhibiting calcium signaling using 1,2-bis(2-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid and heparin decreased the expression of E-selectin. Also, LA-mediated nuclear factor kappa B activation and E-selectin gene expression were suppressed by Mn (III) tetrakis (1-methyl-4-pyridyl) porphyrin pentachloride (a superoxide scavenger), N(G)-monomethyl-l-arginine (an endothelial nitric oxide synthase inhibitor), and 5,10,15,20-tetrakis (4-sulfonatophenyl) porphyrinato iron (III) chloride (a peroxynitrite scavenger). LA exposure resulted in increased nitrotyrosine levels, as observed by Western blotting and immunofluorescence. Our data suggest that the proinflammatory effects of LA can be mediated through calcium and peroxynitrite signaling. | Ramadan MF, Mörsel JT (2003) Determination of the lipid classes and fatty acid profile of Niger (Guizotia abyssinica Cass.) seed oil. Phytochemical analysis : PCA 14, 366-370 [PubMed:14667063] [show Abstract] Niger seeds (Guizotia abyssinica Cass.), which are of interest as a new source of vegetable oils, were subjected to Soxhlet-extraction with n-hexane and the extract analysed using a combination of CC, GC, TLC and normal-phase HPLC. The total lipid content was ca. 300 mg/g seed material, and the fatty acid profile showed a high content of linoleic acid (up to 63%) together with palmitic acid (17%), oleic acid (ca. 11%), and stearic acid (ca. 7%). CC separation over silica gel eluted with solvents of increasing polarity yielded 291 mg/g of neutral lipids, 5.76 mg/g of glycolipids, and 0.84 mg/g of phospholipids. GC analysis showed that the major fatty acid present in all lipid classes was linoleic acid together with minor amounts of palmitic, oleic and stearic acids. Polar lipid fractions, however, were characterised by higher levels of palmitic acid and a lower content of linoleic acid. Phospholipid classes separated by normal-phase HPLC consisted of phosphatidylcholine (ca. 49%), phosphatidylethanolamine (22%), phosphatidylinositol (14%), phosphatidylserine (ca. 8%), and minor amounts (2-3%) of phosphatidylglycerol and lysophosphatidylcholine. | Wulferink M, González J, Goebel C, Gleichmann E (2001) T cells ignore aniline, a prohapten, but respond to its reactive metabolites generated by phagocytes: possible implications for the pathogenesis of toxic oil syndrome. Chemical research in toxicology 14, 389-397 [PubMed:11304127] [show Abstract] The most basic arylamine, aniline, belongs to a class of compounds notorious for inducing allergic and autoimmune reactions. In 1981 in Spain, many people succumbed to toxic oil syndrome (TOS), a disease caused by ingestion of cooking oil contaminated with aniline. Indirect evidence points toward an immune pathogenesis of TOS driven by T lymphocytes, but it is unclear to which antigens these cells could react. Here, using the popliteal lymph node (PLN) assay in mice, we analyzed the sensitizing potential of aniline, its metabolites, and some of the aniline-coupled lipids detected in the contaminated cooking oil. Whereas aniline itself and its non-protein-reactive metabolites nitrobenzene, p-aminophenol and N-acetyl-p-aminophenol, failed to elicit PLN responses, its reactive metabolites nitrosobenzene and N-hydroxylaniline did. The aniline-coupled lipids, namely, linoleic anilide and linolenic anilide, and a mixture of fatty acid esters of 3-(N-phenylamino)-1,2-propanediol, all implicated in TOS, induced significant PLN responses, whereas the respective aniline-free lipids, linoleic acid, linolenic acid, and triolein, did not. Hence, the aniline moiety plays a crucial role in the immunogenicity of the aniline-coupled lipids of TOS. PLN responses to the reactive aniline metabolites and the one aniline-coupled lipid that was tested, linolenic anilide, were T-cell-dependent. Secondary PLN responses to nitrosobenzene were detectable not only after priming with nitrosobenzene but, in some experiments, also after priming with linolenic anilide. This suggests that the aniline moiety was cleaved from the aniline-coupled lipid and metabolized to the intermediate nitrosobenzene that generated the prospective neoantigens. Consistent with this, in lymphocyte proliferation tests in vitro, T cells primed to nitrosobenzene reacted in anamnestic fashion to white bone marrow cells (WBMCs) pulsed with aniline. Hence, we propose that aniline is a prohapten that can be metabolized by WBMCs, which form neoantigens that are recognized by T cells. The possible significance of these findings for the pathogenesis of TOS is discussed. | Spiteller G (2001) Peroxidation of linoleic acid and its relation to aging and age dependent diseases. Mechanisms of ageing and development 122, 617-657 [PubMed:11322990] [show Abstract] Cell proliferation, cell injury and aging are connected with changes in the cell membrane structure. Apparently these changes activate, in mammalian as well as in plant cells, lipases which liberate polyunsaturated fatty acids (PUFAs). PUFAs are the substrates for lipoxygenases which convert them to corresponding hydroperoxides (LOOHs). Lipoxygenases commit suicide by releasing iron ions. LOOHs react with iron ions to generate radicals. Thus, a nonenzymic lipid peroxidation process (LPO) is induced. It is speculated that the change from enzymic to nonenzymic LPO is connected with the switch from apoptosis to necrosis and that LOOHs produced in enzymic reactions are degraded specifically to signal compounds which induce physiological responses, while nonenzymic reactions seem to induce generation of reactive oxygen species, cell death and age related diseases. Enzymic and nonenzymic LPO processes concern all PUFAs not only arachidonic acid. The main PUFA in mammals is linoleic acid. Since these products serve signalling functions, different degradation paths of linoleic-hydroperoxides are described in detail and the physiological properties of LPO products are discussed in relation to aging and age related diseases. | Fitch CD, Cai GZ, Shoemaker JD (2000) A role for linoleic acid in erythrocytes infected with Plasmodium berghei. Biochimica et biophysica acta 1535, 45-49 [PubMed:11113630] [show Abstract] Unesterified fatty acids were measured in mouse erythrocytes infected either with chloroquine-susceptible (CS) or with chloroquine-resistant (CR) lines of Plasmodium berghei. This work was undertaken to identify candidates for the lipid involved in ferriprotoporphyrin IX (FP) polymerization. Linoleic, oleic, palmitic, and stearic acids were quantified by gas chromatography/mass spectrometry. In total, they increased 4-fold with CS infections and 6-fold with CR infections. Treating infected mice with chloroquine did not affect the amounts of unesterified fatty acids in erythrocytes. Of the four fatty acids, only linoleic acid increased disproportionately to the total. It increased 16-fold for the CS line and 35-fold for the CR line. The method could detect monoglycerides but they were below the limit of detection. It could not detect diglycerides, triglycerides or phospholipids. Triglycerides and phospholipids have been tested previously, however, and found to be ineffective at promoting FP polymerization. Therefore, other than linoleic acid, the lipids most likely to be involved in FP polymerization are diglycerides. We tested dilinoleolyglycerol in the present work and found it to be an effective promoter of FP polymerization. These results suggest that linoleic acid or a diglyceride containing it has the critical role of promoting FP polymerization in malaria parasites. | Marquet A, Larraga V, Diez JL, Amela C, Rodrigo J, Muñoz E, Pestaña A (1984) Immunogenicity of fatty acid anilides in rabbits and the pathogenesis of the Spanish toxic oil syndrome. Experientia 40, 977-980 [PubMed:6205897] [show Abstract] Fatty acid anilides, the major xenobiotic found in the cooking oils responsible for the Spanish toxic oil syndrome, are immunogenic for rabbits as ascertained by a skin test reaction, the characterization of specific antibodies against anilides and the immunofluorescent detection of 'anilide dependent antigens' in tissue slices from treated animals. |
|