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PubMed2003

Molecular tagging of erucic acid trait in oilseed mustard (Brassica juncea) by QTL mapping and single nucleotide polymorphisms in FAE1 gene.

Molecular mapping and tagging of the erucic acid trait (C22:1) in Brassica juncea was done by a candidate gene approach. Two QTLs underlying the variation of seed erucic acid content were assigned to two linkage groups of a B. juncea map using a doubled haploid (DH) mapping population derived from high x low erucic acid F(1) hybrid. Two consensus primers corresponding to the full-length Fatty Acid Elongase 1 ( FAE1) gene, reported to be involved in the elongation of C18:1 to C22:1, were designed. PCR amplification and subsequent cloning and sequencing identified two FAE1 genes ( FAE1.1 and FAE1.2) in both high and low erucic acid mustard lines. Sequence alignment of corresponding FAE1 genes between high and low erucic acid mustard lines identified four substitution type single nucleotide polymorphisms (SNPs) in FAE1.1 and three in FAE1.2. Using the SNuPE method of SNP genotyping, these two genes were mapped to two independent loci that co-segregated with the two QTLs governing the erucic acid trait. Association of wild ( E1E2) and mutant ( e1e2) haplotypes of two FAE1 genes with erucic acid variation in two segregating populations revealed that the e1e1e2e2 genotype identified low erucic acid individuals (<2%) and E1E1E2E2 identified individuals with highest erucic acid content (>40%). The E1e1E2e2 heterozygote was found to be intermediate in phenotype. The applicability of these SNPs in marker-assisted manipulation of the erucic acid trait was verified by genotyping a set of contrasting germplasm of B. juncea belonging to two distinct gene pools (Indian and east European) and other oil-yielding Brassica species.

Acetyltransferases↗
PubMed1977

Erucic acid and phospholipids of newborn rat heart cells in culture.

Erucic acid (delta 13-docosenoic acid), labeled with 14C in the 1- or 14-position, was incorporated into fetal calf serum and fed to beating, neonatal rat myocardial cell in culture. Uptake of the docosenoic acid during the first 6 hr of incubation was 41 nM/hr/mg protein in 7-day old cells and 29 nM/hr/mg protein in 14-day old cells. Fifty-seven percent of the 14C-activity was taken up from the medium in 24 hr, of which 77% was in the cells and 23% was unaccounted for. Of the 14C-activity taken up, 26% was in extractable lipid, with two-thirds in neutral lipid and one-third in phospholipid. Within the neutral lipid fraction, 88% of the 14C-activity was present in triglycerides; while in phospholipids, 66% of the 14C-activity was in phosphatidylcholine (PC); 14% in phosphatidylethanolamine (PE); 6% in sphinogomyelin (SPH) and 1% or less in cardiolipin (DPG). PC had the highest specific activity, followed by SPH and PE. The specific activity of PE was one-half that of SPH when the 14C-erucic acid substrate was labeled at the carboxyl position, but increased to equal that of SPH when the substrate was labeled at the double bond. The fatty acids of PC, PE, and SPH were influenced by erucic acid in the growth medium, but the amounts of each phospholipid were not affected. It is proposed that the altered fatty acid composition associated with incorporation of erucic acid or its metabolites into PC, PE, and SPH may affect integrity and function of heart cell membranes.

Animals↗
PubMed1989

Dietary erucic acid therapy for X-linked adrenoleukodystrophy.

We investigated the biochemical and clinical efficacy of dietary erucic acid (C22:1) therapy for X-linked adrenoleukodystrophy (ALD). In a double-blind crossover study of patients who were on chronic oleic acid (C18:1) therapy, addition of erucic acid to the diet led to a further reduction in plasma hexacosanoic acid (C26:0) concentration. We treated 12 newly diagnosed ALD patients with a diet enriched with erucic acid and oleic acid for 2 to 19 months. Mean plasma C26:0 concentration decreased to normal by 4 weeks, and the C26:0 composition of plasma sphingomyelin and phosphatidylcholine became normal by 4 months on therapy. Fatty acid analysis of postmortem tissues from 1 boy treated for 10 months suggested that dietary erucic acid entered the heart, liver, adrenal gland, and brain. Eight patients remained on treatment long enough (mean, 12 +/- 3 months) to evaluate their clinical response; 6 of these patients with moderate to advanced disease deteriorated neurologically or showed progression of white matter disease on brain magnetic resonance imaging whereas 2 mildly affected patients remained clinically stable after 10 and 19 months. No adverse effects of the diet occurred. We conclude that dietary erucic acid therapy is effective in lowering plasma C26:0 to normal in ALD patients, and may prevent further demyelination in some mildly affected boys.

Adrenoleukodystrophy↗
PubMed1986

Effects of feeding high-fat diets to rats: metabolism of erucic acid (C 22:1 n-9) in the perfused liver and secretion of metabolites to the perfusate.

The liver metabolism of erucic acid, 22:1 n-9, was studied in rat livers perfused with 14-14C-labelled erucic acid for 15 and 60 min, determining the distribution of radioactivity in the perfusate and in the lipids of the liver cell organelles. The rats were adapted to a high-fat diet containing either partially hydrogenated marine oil (PHMO) or palm oil (PO), both adjusted to a 10% content of linoleic acid. The results showed an efficient uptake and metabolism of erucic acid with the secretion to the perfusate medium of labelled free fatty acids other than erucic acid, labelled phospholipids as well as water soluble oxidation products. Only minor amounts of secreted labelled triglycerides were found within 60 min of perfusion. In the liver, labelled lipids accumulated in the endoplasmic reticulum, after 15 min mainly as free fatty acids, after 60 min as triglycerides. The esterification pathway, including the erucic acid given as well as chain-shortened fatty acids, seemed to be preferred under the experimental conditions and with adequate linoleic acid in the diet. A chain shortening of erucic acid probably took place in both peroxisomes and mitochondria shown by the presence of labelled 18:1 and 20:1 in the organelle-bound phospholipids. A chain shortening was found in both dietary groups, and is assumed to be an affect of the adaptation to a high-fat diet rather than an effect of dietary very long chain monoenoic fatty acids. Somewhat higher levels were found in the PHMO group, but the difference in the dietary fat was not a major factor in the liver lipid adaptation.

Animals↗
PubMed1979

Effects of high and low erucic acid rapeseed oils on energy metabolism and mitochondrial function of the chick.

Duplicate experiments were conducted to compare energy utilization, growth, cardiac mitochondrial oxidative phosphoryl,tion, and mitochondrial membrane fatty acid composition of chicks fed diets containing 20 parts of high erucic acid rapeseed oil (HER), low erucic acid rapeseed oil (LER) or sunflower seed oil (SFO) for 24 days. Chicks fed diets containing HER deposited less fat and utilized energy less efficiently (kcal gained/kcal consumed) than chicks fed diets containing either LER or SFO. Energetic efficiency and fat deposition of chicks pair-fed diets containing LER were significantly lower than for chicks fed diets containing SFO. Cardiac mitochondria isolated from chicks fed diets containing either HER or LER for 24 days had significantly reduced ADP/O ratios and reduced rates of ATP synthesis utilizing pyruvate and malate as the respiratory substrates when compared with mitochondria isolated from chicks fed SFO. Diet induced transitions in fatty acid composition of cardiac mitochondrial membranes were also observed. The composition of fat ingested affected the fatty acid composition of mitochondrial diphosphatidyl glycerol more than the fatty acid composition of phosphatidyl choline or phosphatidyl ethanolamine. The linoleic acid content of mitochondrial diphosphatidyl glycerol was lower and the gadoleic acid and erucic acid content higher for chicks fed diets containing rapeseed oils than for chicks fed SFO containing diets. These studies indicate that a complex dynamic mechanism exists associating dietary fat with mitochondrial structural-functional changes and energetic efficiency in the growing chick.

Animals↗
PubMed1980

Effect of erucic acid on the phospholipid molecular species compositions of the rat heart and liver.

Erucic acid was not incorporated into phosphatidylcholine or phosphatidylethanolamine, but was into diphosphatidylglycerol and sphingomyelin in both the heart and liver of male Wistar rats fed erucic acid for 20 days. A remarkable difference between the heart and liver was found in the molecular species composition of phosphatidylcholine. The 1-stearoyl//2-arachidonoyl species of phosphatidylcholine in the heart was maintained at a higher level in rats fed the erucic acid diet than in rats fed a low fat diet. There was no difference in this molecular species content of cardiac and hepatic phosphatidylethanolamine between rats fed erucic acid and low fat diets. The level of erucic acid incorporated into triacylglycerols and free fatty acids in heart was higher than in the liver.

Animals↗
PubMed2004

Identification of the linkage relationship between the flower colour and the content of erucic acid in the resynthesized Brassica napus L.

Brassica napus variety Quantum (yellow flower and low erucic content) as the female parent was crossed with a resynthesized Brassica napus line No. 2127-17 (white flower and high erucic content). The segregation ratios of the flower colour and the erucic acid content were analyzed in the F1, BC1, F2, and DH (doubled haploid) populations. The results indicated that the white flower was dominant over yellow and the erucic acid content was additively inherited. Both traits fit with a monogenic inheritance model, respectively. There were strong evidences to support the linkage relationship between the flower colour and the erucic acid content in the C-genome of B. napus with a recombination frequency of 5.8% in the DH population. The BSA (bulked segregant analysis) strategy was employed to identify random amplified polymorphic DNA (RAPD) marker linked to the genes for the flower colour and erucic acid content in the DH population. Of 685 arbitrary 10-base pair (bp) primers, one primer S92 generated a RAPD marker S92(-1400) that was tightly linked to the genes for the yellow flower and the low erucic acid content in the C-genome of B. napus L. The genetic distance of the genes for yellow flower and the low erucic acid content was 2.2 cM and 5.4 cM from the marker S92(-1400), respectively.

Brassica napus↗
PubMed1983

Evidence for a negative modulating effect of erucic acid on the peroxisomal beta-oxidation enzyme system and biogenesis in rat liver.

In male rats fed a 30 cal% high-erucic acid (22:1 (13) (cis] rapeseed oil diet for 4 weeks a transient, small increase in peroxisomal beta-oxidation was observed in liver homogenates and isolated peroxisomes after approximately 1 week. Morphometric analysis revealed a progressive decrease in the average size of the liver peroxisomes (by approx. 20%), as well as their volume fraction (by more than 40%). A negative dose-response was observed when peroxisomal beta-oxidation was determined in animals fed rapeseed oil diets with a variable content of erucic acid. When erucic acid was given as subcutaneous injections the peroxisomal beta-oxidation decreased, in both liver homogenates and isolated peroxisomes. In contrast to recent proposals, our findings indicate that the amount of erucic acid cannot account for the small increase in peroxisomal beta-oxidation observed in the liver of rats adapted to a diet containing 30 cal% rapeseed oil with a high content of this fatty acid. In fact, by the selected criteria erucic acid seems to have a negative modulating effect on both the peroxisomal beta-oxidation enzyme system and biogenesis.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1976

Relationship between erucic acid and myocardial changes in male rats.

The back and belly fat of pigs fed a diet containing 20% by wt rapeseed oil (22% erucic acid) for 16 weeks was rendered into oil. This rendered pig fat, which contained 5.6% erucic acid, was fed to male rats in three separate experiments at 20% by wt of the diet for 16 weeks. In experiment I rendered pig fat was compared only to Brassica campestris var. Span rapeseed oil containing 4.8% erucic acid. In experiments II and III, rendered pig fat was compared to commercial lard containing 0.2% docosenoic acid, commercial lard to which 5.4% free erucic acid was added, and Span rapeseed oil. There was no significant (P less than 0.01) differences observed in the level of erucic acid in the hearts of rats fed diets of rendered pig fat, Span rapeseed oil, or commercial lard plus erucic acid. However, the incidence (P less than 0.001) and severity (P less than 0.01) of cardiac lesions were significantly higher in Span rapeseed oil fed rats compared to rats fed control diets. The number of rats affected or the severity of lesions in the rendered pig fat fed group was not significantly different from controls. The results of this study indicate that the myocardial lesions associated with feeding 20% rapeseed oil diets are not related to the content of erucic acid per se. The possible reasons why rapeseed oil causes cardiac lesions in rats are discussed. It is suggested that a triglyceride imbalance in the oil might play an important role in causing these lesions in rats.

Animals↗
PubMed1975

[Oxidation of erucic acid and erucyl-CoA by isolated rat heart mitochondria: comparison to oleic acid].

The oxidation of [14 14-C] or [1 14-C] erucic acid by isolated mitochondria from Rat heart has been studied and compared with that of [10 14-C] oleic acid in varying conditions of incubation. Erucic acid is converted to CO2 and acid-soluble compounds much more slowly than oleic acid. The acid-soluble compounds which have been identified are acylcarnitines, ketone bodies and intermediates from the Krebs cycle; they are found in similar proportions for both substrates. Moreover, the oxidation rate of erucyl-CoA is comparable, if not equal, to that of oleyl-CoA in the same conditions. These results are discussed here. They lead to the conclusion that erucic acid is oxidized by isolated Rat heart mitochondria through the beta oxidation pathway, and that its oxidation is limited owing to its slow activation rate.

Animals↗
PubMed1996

Effect of erucic acid on platelets in patients with adrenoleukodystrophy.

In a clinical trial for the management of adrenoleukodystrophy, we analyzed the effect of erucic acid (a component of Lorenzo's oil) on platelet number, fatty acid composition, and function. Analysis of variance was performed to compare platelet counts before starting treatment with Lorenzo's oil and at 6 and 12 months. We measured platelet fatty acid composition in subjects and control patients and correlated these values with their platelet counts using discriminant analysis. After 6 months, the mean platelet count decreased from 247,000/mm3 to 169,000/mm3 (+/- 1 standard deviation 58,000,n =39), P < 0.0001 compared to 18 subjects on a control diet having a mean baseline platelet count of 259,000/mm3 (+/- 1 standard deviation 67,000, n = 19) and at 6 months 267,000/mm3 (+/- 1 standard deviation 71,000). We found at P < 0.05 that the platelet counts showed a strong inverse relationship with erucic acid levels and other omega 9 fatty acids that form from the administration of the erucic acid component of Lorenzo's oil. Morphologic and platelet sizing measurements suggest that the physical properties of platelets may also be affected by erucic acid. Our studies show that the ingestion of erucic acid affects platelet biology. This indicates that platelet counts and properties are influenced by monounsaturated fatty acids, in addition to the well-known effects of polyunsaturated fatty acids. In areas of the world where erucic acid is widely ingested, the biology of platelets in these populations may be affected.

Adrenoleukodystrophy↗
PubMed1980

Evidence of accumulation of ceramides containing [14C]nervonic acid in the rat lung following injection of [14C]erucic acid.

A mixture of albumin-bound [14C]erucate and [3H]oleate was injected into rats fed a stock pellet diet containing 4% by weight of lipid. Chylomicrons containing the same labelled fatty acids were also injected into rats fed diets containing 15% by weight of rapeseed oil (48% of erucic acid), canbra oil (less than 5% of erucic acid) or ground nut oil (no erucic acid). Lung lipids were analyzed at various times after injection. In all cases, except in the rapeseed oil diet group, 14C radioactivity of lung 'monoacylglycerol' was ten times higher than 3H radioactivity. More than 85% of this 14C radioactivity was found in nervonic acid (24 : 1). It was shown by TLC and GLC analysis that 85-90% of the 14C radioactivity of this fraction was in ceramides (N-acyl-4-sphingenine). Ceramides containing [14C]nervonic acid disappeared from the lung with time and their incorporation with time into sphingomyelin was also observed. The absence of accumulation of 3H and 14C (18 : 1) in ceramides showed that oleic acid was not incorporated into sphingomyelin in the same way as nervonic acid. In the rapeseed oil diet group, there was no accumulation of 14C radioactivity in ceramides and conversion of erucic acid into nervonic acid was less, and into oleic acid more, than in other diet groups indicating a possible enzyme adaptation.

Animals↗
PubMed2005

Increased levels of erucic acid in Brassica carinata by co-suppression and antisense repression of the endogenous FAD2 gene.

Erucic acid and its derivatives represent important industrial feedstock compounds, and there is an increasing demand for the production of high erucate oils in this regard. Our goal therefore, is to develop high erucic acid (HEA) Brassicaceae lines with increased proportions of erucic acid and very long-chain fatty acids (VLCFAs). We proposed that oleate availability may be a rate-limiting factor in the biosynthesis of erucic acid. We have tried to address this question by manipulating the expression of the endogenous FAD2 gene in B. carinata using co-supression and antisense approaches. Both methods resulted in transgenic lines exhibiting decreased proportions of polyunsaturated C18 fatty acids (18:2+18:3) and concomitant and significantly increased proportions of 18:1, 22:1 and total VLCFAs. Co-suppressed FAD2 B. carinata lines exhibited 3-18% decreases in 18:2, 22-49% decreases in 18:3 and significantly increased proportions of 18:1 (36-99%), 22:1 (12-27%) and VLCFAs (6-15%). Transgenic B. carinata lines developed using an antisense FAD2 approach exhibited decreased proportions of 18:2 and 18:3 (9-39% and 33-48%, respectively) and significantly increased proportions of 18:1 (54-130%), 22:1 (5-19%) and VLCFAs (6-21%). The possibility of using these approaches to produce prototype transgenic germplasm of the Brassicaceae accumulating seed oils with improved proportions of erucic and other VLCFAs is discussed.

Brassica↗
PubMed1982

[Modes of action of a shortening system for erucic acid at the mitochondrial level of rat liver].

In this work, were studied the conditions of erucic acid (cis-docosenoic, n-9) shortening by using Rat liver mitochondrial preparations which were incubated in vitro with [14-14C] erucic acid (22:1), with inhibitors of the respiratory chain (rotenone, cyanide) or not, with activators of either the shortening reaction (NAD+, NADP+), or beta-oxidation (malate, carnitine, cytochrome c) or not. The shortening activity was measured by the amount of 14C radioactivity recovered in the shorter fatty acids formed (20:1, 18:1, 16:1) when beta-oxidation was inhibited. The beta-oxidation activity was measured by the amount of 14C recovered in the acid-soluble products (P A S). The incubations were performed under conditions which were the least favourable to peroxysomal activity. Data showed that, with increasing amounts of albumin, which inhibits peroxysomal activity, increasing amounts of shorter fatty acids (20:1, 18:1, 16:1) were formed from erucic acid. This shortening reaction was strongly stimulated by NAD+, more than by NADP+; it was also stimulated by cytochrome c and much more when both NAD+ and cytochrome c were added. Similar data were observed in beta-oxidation, except that practically NADP+ did not exhibit any stimulating effect. Oxidation of NADH by mitochondria only occurred when cytochrome c was added to the medium and was not modified by the addition of ADP or rotenone. These data show that liver mitochondria are capable of shortening erucic acid, as are peroxysomes. This shortening reaction is highly NAD+-dependent and seems to be localized outside the matrix. This system could constitute a second route for utilization of fatty acids in mitochondria, besides the well-known path of beta-oxidation.

Animals↗
PubMed1979

The effect of feeding rats with partially hydrogenated marine oil or rapeseed oil on the chain shortening of erucic acid in perfused heart.

1. The metabolism of [14(-14)C]erucic acid and [U-14C]palmitic acid was studied in perfused hearts from rats fed diets containing hydrogenated marine oil, rapeseed oil or peanut oil for three weeks. 2. [14C]Erucic acid was shortened to [14C]eicosenoic acid (20 : 1, n -- 9) and [14C]oleic acid (18 : 1, n -- 9) in perfused rat hearts from all diet groups. The rapeseed oil diet caused a three-fold increase and the marine oil diet a four-fold increase in the amount of chain-shortened products recovered in heart lipids at the end of perfusion, compared to peanut oil diet. 3. The content of C16:1, C18:1 and C20:1 fatty acids was increased in heart lipids of rats fed hydrogenated marine oil or rapseed oil diet, compared to peanut oil diet. 4. Feeding hydrogenated marine oil or rapeseed oil to the rats induced a 85% increase in catalase activity, a 20% increase in the activity of cytochrome oxidase and a 30--40% increase in the content of total CoA in the heart compared to rats fed peanut oil diet. 5. It is suggested that [14(-14)C]erucic acid is shortened by the beta-oxidation system of peroxisomes in the heart. The increased chain shortening in the hearts from animals fed rapeseed oil or partially hydrogenated marine oil for three weeks may be an important part of an adaptation process.

Animals↗
PubMed1984

Influence of dietary rapeseed oil and erucic acid upon myocardial performance and hemodynamics in rats.

Rats fed rapeseed oil, pure erucic acid, or a control diet of sunflowerseed oil during 24-26 weeks were studied for effects upon mechanical behavior of the isolated perfused heart and upon myocardial performance and hemodynamics in intact animals both under basal and stimulated conditions. In spite of focal myocardial fibrotic lesions due to rapeseed oil, no changes were found with respect to the intrinsic myocardial contractility in vitro and and in vivo. After inotropic intervention, only the rapeseed oil fed animals showed less contractile reserve capacity. The absence of this effect in the erucic acid-treated animals is in agreement with the histological studies showing no epicardiac fibrotic lesions in these animals. It appears that erucic acid is able to interfere with the contractile system of the peripheral vascular system. Both in the rapeseed oil-treated group and the erucic acid-treated group, the vasoconstrictor response toward norepinephrine was profoundly reduced. In all three oil fed groups, isoproterenol reduced myocardial contractility which has been attributed to a lowered perfusion pressure in the coronary blood supply of the myocardium with simultaneous increased energy demand. Neither rapeseed oil nor erucic acid feeding led to electrocardiographic changes in comparison with the control sunflowerseed oil group. It is concluded that rapeseed oil and not erucic acid is responsible for loss of contractile reserve capacity without changes in the myocardial conductance system and further, that erucic acid might interfere with the peripheral vascular system. Finally, it appears that a fat rich diet might result in reduced myocardial function during a state of energy demand coupled with a blood pressure decrease.

Animals↗
PubMed1978

Effects of rapeseed oil compared to hydrogenated marine oil in rats. Histopathological effects of erucic acid and isomers on the heart.

In a recent review on the role of fats in human nutrition Vergroesen and Gottenbos (1975) emphasize, that the presence of erucic acid isomers in hydrogenated marine oils (HMO) may constitute a toxicological problem as serious as erucic acid in rapeseed oil (RSO). On the contrary Christophersen et al. (1976) stress, that these fatty acids in HMO represent a minor toxicological problem, and that conclusions drawn from HMO to RSO are questionable. Preliminary studies at our institute indicate lipidosis in the heart both in rats fed RSO and HMO, containing equivalent amounts of erucic acid and erucic acid isomers respectively. Further experiments of longer duration are performed with HMO and RSO in order to compare the effect on the heart, especially in relation to the formation of cell necrosis.

Animals↗