SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Trans-isomers of erucic acid (especially brassidic acid) do not incorporate in rat adipose tissue as well as erucic acid. Brassidic acid is partially converted into shorter trans-monoenes (mainly C18:1) since these acids have been identified in adipose tissue of rats fed brassidic acid as the only source of trans-fatty acid in the diet.
Microsomes and mitochondria of liver, kidneys, and heart were incubated with [14-(14)C] erucic acid in three assay media: one favorable for chain elongation (NADPH + KCN), another favorable for beta-oxidation and the last one for shortening (NADP + KCN). Elongating reactions occurred mainly in microsomes, those of kidneys being very active; the mitochondria also showed some activity, heart mitochondria being, however, more active than the microsomes, when considering the amount of erucic acid activated. In the medium for beta-oxidation, practically no shortened fatty acids were found. On the contrary, when beta-oxidation was inhibited, and in the presence of NADP, the formation of shorter monoenes, probably in the outer membrane of the mitochondria, was observed, namely eicosenoic acid in high amount, oleic acid and hexadecenoic acid. Mitochondria from liver were very active as were those of heart, when compared with the quantity of activated erucic acid. In heart, the mitochondria shortened erucic acid into oleic acid and hexadecenoic acid, which were then probably used as energy substrates. With carnitine and without NADP, shortened fatty acids were formed in the mitochondria of liver, probably by the first reactions of beta-oxidation. In this case, the proportions of oleic acid and hexadecenoic acid were higher than with NADP alone. In the presence of carnitine and NADP, the level of the chain-shortening reaction did not differ from that observed with NADP alone. It appears, therefore, that the activated erucic acid is mainly directed towards shortening reactions and not towards transfer reactions across the mitochondrial membranes.
Two groups of rats were fed diets containing 20% by weight of either partially hydrogenated marine oil supplemented with sunflower seed oil (PHMO) or palm oil (PO) for 8 wk. Using a liver perfusion system, the effect of dietary long chain monoenoic fatty acids on the uptake and metabolism of [14-14C]erucic acid was studied. The perfusion times were 15 and 60 min, respectively. The two groups showed equal ability for erucic acid uptake in the liver but differed in the channeling of the fatty acids into various metabolic pathways. A higher metabolic turnover of 22:1 in the PHMO livers relative to the PO livers was demonstrated by an increased recovery of total [14C]labeling in the triglyceride (TG) and phospholipid (PL) fractions, already evident after 15 min of perfusion. The chain-shortening capacity was highest in the PHMO group, reflected by a higher [14C]18:1 incorporation in both TG and PL, and increasing from 15 to 60 min of perfusion. The amount of [14C]18:1 found in PL and TG after 60 min of perfusion of livers from rats fed PO corresponded to that shown for the PHMO group after 15 min. The PL demonstrated a discrimination against 22:1 compared to TG, and, when available, 18:1 was highly preferred for PL-synthesis. The total fatty acid distribution in the TG, as determined by gas liquid chromatography (GLC), reflected the composition of the dietary fats. In the total liver PL, 22:1 and 20:1 were present in negligible amounts, although the PHMO diet contained 12-13% of both 22:1 and 20:1. In the free fatty acid fraction (FFA), the major part of the radioactivity (approximately 80%) was [14-14C]erucic acid, and only small amounts of [14C]18:1 (less than 2%) were present, even after 60 min of perfusion. The shortened-chain 18:1 was readily removed from the FFA pool and preferentially used for lipid esterification.
Experiments were conducted to compare energy utilization, growth and tissue composition of chicks fed diets containing 10 or 20 parts of either high erucic acid rapeseed oir 24 days. Results showed that chicks fed diets containing 10 or 20 parts LER grew at the same rate, utilized energy just as efficiently, had similar heart to body weight ratios and levels of heart lipids equal to or less than chicks fed comparable diets containing SFO. The substitution of 10 or 20 parts HER for an equienergetic amount of SFO depressed gorwth, feed consumption and carcass fat deposition but had no effect on level of cardiac lipid or relative heart size when fed from 4 to 11 days of age. When fed from 4 to 25 days of age, chicks fed 20 parts HER grew slower, consumed less feed, and when pairfed, deposited less carcass fat, utilized energy less efficiently, had increased heart to body weight ratios but a lower level of cardiac lipid than chicks fed comparable diets containing SFO. Irrespective of the type of rapeseed oil or of the age of the chick, heart lipids contained less erucic acid than carcass fat, indicating that chick heart is as capable of disposing of erucic acid as carcass tissue. It was also found that irrespective of the diet fed, a greater percentage of erucic acid appeared to be oxidized than of eicosenoic acid.
In Brassicas, the Fatty Acid Elongation1 (FAE1) gene product, a 3-ketoacyl-CoA synthase, is the first in a 4-enzyme complex involved in the synthesis of erucic acid from oleic acid. The FAE1 homologue from Brassica juncea cv. Pusa Bold was cloned in a binary vector both in sense and antisense orientations under the control of the CaMV35S promoter. The recombinant binary vectors were used to transform B. juncea cv. RLM 198 via Agrobacterium tumefaciens. The presence of the transgene was confirmed by polymerase chain reaction and Southern hybridization. Northern and western analyses showed the expression of the gene and protein, respectively, in the transgenic plants. Analyses of the fatty acid profile of the seed oil from homozygous T4 generation seeds revealed that over-expression of the FAE1 gene caused a 36% increase in the percent of erucic acid (37-49% compared to 36% in untransformed control). The down-regulation of FAE1 caused an 86% decrease in the percent of erucic acid to as low as 5% in the seed oil of transgenic plants. Thus, it is clearly possible to alter erucic acid content of mustard by altering the expression level of the FAE 1 gene.
Ten Japanese boys with childhood adrenoleukodystrophy (ALD), one adult patient with adrenomyeloneuropathy (AMN), and two presymptomatic ALD boys were treated with dietary erucic acid (C22:1) for more than 12 months; except in a case of childhood ALD patient who died 7 months after beginning erucic acid therapy. During erucic acid therapy, the serum levels of very long-chain fatty acid (VLCFA) (C24:0/C22:0) decreased within 1-2 months in all patients, and these levels in four of the patients decreased to the normal range. Neurological examination and MRI findings in all 10 of the childhood ALD patients showed progression of the disease while they were receiving the dietary therapy. However, the mean interval between the onset of awkward gait and a vegetative state in diet-treated patients was significantly longer than that in the untreated patients. One AMN patient showed slight improvement of spastic gait and lessened pain in the lower limbs due to spasticity. The two presymptomatic ALD boys remained intact on clinical examination and on MRI findings for 38 and 23 months, respectively, after starting the diet.
The possibility of dietary C18 unsaturated fatty acids double bonds biohydrogenation, which normally occurs in ruminants, has been investigated in the case of erucic acid (22:1 n-9 cis). The results have shown that, while oleic acid is always converted into hydrogenation intermediates and stearic acid, to various extent, erucic acid does not undergo hydrogenation process, unrelated to the incubation conditions applied. Data are discussed on the basis of the different structure of erucic and oleic acids.
Cardiac erucic acid metabolism has been studied with beating heart cells in culture. It has been shown that erucate is taken up by these cultured cardiac myocytes. These cells are unable to oxidize it directly but require delaying intermediary steps to shorten the erucic acid chain before its complete oxidation. This long latency time of erucate oxidation would explain its accumulation within the different cellular lipid classes. It is suggested that the occurrence of large amounts of erucate in the different phospholipids might affect cellular and mitochondrial membrane structures. Evidence is reported that erucate does not affect the oxidative capacity of the myocardial cell but because of its accumulation dilutes other fatty acids which will then be oxidized at a lower rate.
Laying pullets were fed a diet supplemented with three percent of either high-erucic acid rapeseed (HEAR) oil or low-erucic acid rapeseed (LEAR) oil for 39 weeks. Egg production for the period was 78.8 and 80.1% by the birds fed the respective oils. Average egg weights were 56.8 and 58.7 g. respectively. Gains in body weight, liver weight and adrenal gland weight were similar with the two types of oil fed. Feed consumption was similar for the two groups of birds. The efficiency of utilization of the diet containing HEAR oil was accordingly lower than that of the diet containing LEAR oil. In the birds fed HEAR and LEAR oil respectively mortality attributed to metabolic disorders of the reproductive system, liver, and kidney was 3.3% and 1.2%. Mortality from other causes in the birds fed the two oils was 3.2 and 3.8% of the original populations.
The metabolism of long chain unsaturated fatty acids was studied in cultured fibroblasts from patients with X-linked adrenoleukodystrophy (ALD) and with neonatal ALD. By using [14-14C] erucic acid (22:1(n-9)) as substrate it was shown that the peroxisomal beta-oxidation, measured as chain shortening, was impaired in cells from patients with neonatal ALD. The beta-oxidation of adrenic acid (22:4(n-6)), measured as acid-soluble products, was also reduced in the neonatal ALD cells. The peroxisomal beta-oxidation of [14-14C]erucic acid (22:1(n-9)) and [2-14C]adrenic acid (22:4(n-6)) was normal in cells from X-ALD patients. The beta-oxidation, esterification and chain elongation of [1-14C]arachidonic acid (20:4(n-6)) and [1-14C]eicosapentaenoic acid (20:5(n-3)) was normal in both X-linked ALD and in neonatal ALD. Previous studies suggest that the activation of very long chain fatty acids by a lignoceryl (24:0)-CoA ligase is deficient in X-linked ALD, while the peroxisomal beta-oxidation enzymes are deficient in neonatal ALD. The present results suggest that the peroxisomal very long-chain acyl-CoA ligase is not required for activation of unsaturated C20 and C22 fatty acids and that these fatty acids can be efficiently activated by the long chain acyl-(palmityl)-CoA ligase.
Detailed morphometric studies performed in heart tissue from Swiss mice and Wistar rats show that, in comparison with other edible oils, long-term feeding of the new rapeseed oils, poor in erucic acid, do not significantly affect the incidence of myocardial background lesions, in contrast to high-erucic-acid rapeseed oil. The strong predisposition of the Sprague-Dawley rat, however, to develop myocardial necrosis is re-emphasized. The factors underlying this particularity need further clarification. The data presented and the available evidence from experiments involving pigs, monkeys and poultry show that a reduction of the content of erucic acid in rapeseed lipids, as has been achieved by selective plant breeding, considerably improves the nutritional status of the cruciferous oils.
We examined the ability of erucic acid (22:1n-9) to cross the blood-brain barrier (BBB) by infusing [14-14C]22:1n-9 (170 microCi/kg, iv and icv) into awake, male rats. [1-14C]arachidonic acid (20:4n-6) [intravenous (i.v.)] was the positive control. After i.v. infusion, 0.011% of the plasma [14-14C]22:1n-9 was extracted by the brain, compared with 0.055% of the plasma [1-14C]20:4n-6. The [14-14C]22:1n-9 was extensively beta-oxidized (60%), compared with 30% for [1-14C]20:4n-6. Although 20:4n-6 was targeted primarily to phospholipid pools, 22:1n-9 was targeted to cholesteryl esters, triglycerides, and phospholipids. When [14-14C]22:1n-9 was infused directly into the fourth ventricle of the brain [intracerebroventricular (i.c.v.)] for 7 days, 60% of the tracer entered the phospholipid pools, similar to the distribution observed for [1-14C]20:4n-6. This demonstrates plasticity in the ability of the brain to esterify 22:1n-9 in an exposure-dependent manner. In i.v. and i.c.v. infused rats, a significant amount of tracer found in the phospholipid pools underwent sequential rounds of chain shortening and was found as [12-14C]20:1n-9 and [10-14C]oleic acid. These results demonstrate for the first time that intact 22:1n-9 crosses the BBB, is incorporated into specific lipid pools, and is chain-shortened.
Comprehensive investigations were carried out for establishing the biological and nutritional value of low erucic-acid rapeseed oil from a variety of rape called Janpol selected in Poland. The pathophysiological effects of Janpol rapeseed oil were observed after giving it as the only source of fat in the diet or added in different proportions to other edible fats. In all cases the total amount of fat in the diet was 20 p. 100 kcal. The investigations were carried out on 78 young male Wistar rats aged 25 days at the beginning of the experiment. The rats were divided into 7 groups and they were given diets containing: 1) soybean oil; 2) mixed fats; 3) rapeseed oil of high erucic-acid content; 4) mixed fats containing 25 p. 100 of Janpol rapeseed oil; 5) mixed fats with 50 p. 100 of Janpol rapeseed oil; 6) mixed fats with 75 p. 100 of Janpol rapeseed oil; 7) Janpol rapeseed oil only. The experiment lasted 3 months. After its completion the rats were decapitated after 18 hours of starvation. The investigation s included : determination of weight gain, determination of the weight of selected organs (liver-lungs, heart, kidneys, testes, spleen), determination of alkaline phosphatase and pseudocholinesterase activity in the serum, determination of triglycerides and cholesterol in the serum, tests for adrenocortical function, histo-chemical investigations of the liver (alkaline and acid phosphatase, adenosine triphosphatase, fatty infiltration of the liver), macroscopic and microscopic anatomopathological examinations. The authors found the Janpol rapeseed oil caused less pronounced changes in the determined indices of the biological and nutritional evaluation as compared with high-erucic-acid rapeseed oil. Janpol repeseed oil given to experimental animals mixed with other fats in proportions of 25 p. 100 and 50 p. 100 of all fats in the diet, that is 5 p. 100 and 10 p. 100 kcal in the diet derived from Janpol oil gave in most determinations of the investigated parameters results very similar to those observed in animals receiving soybean oil. The results of these investigations show that Janpol rapesed oil can be used for nutrition of man in amounts not exceeding 10 p. 100 of the total caloric content of food.
The fatty acid elongase [often designated FAE or beta-(or 3-) ketoacyl-CoA synthase] is a condensing enzyme and is the first component of the elongation complex involved in synthesis of erucic acid (22:1) in seeds of garden nasturtium (Tropaeolum majus). Using a degenerate primers approach, a cDNA of a putative embryo FAE was obtained showing high homology to known plant elongases. This cDNA contains a 1,512-bp open reading frame that encodes a protein of 504 amino acids. A genomic clone of the nasturtium FAE was isolated and sequence analyses indicated the absence of introns. Northern hybridization showed the expression of this nasturtium FAE gene to be restricted to the embryo. Southern hybridization revealed the nasturtium beta-ketoacyl-CoA synthase to be encoded by a small multigene family. To establish the function of the elongase homolog, the cDNA was introduced into two different heterologous chromosomal backgrounds (Arabidopsis and tobacco [Nicotiana tabacum]) under the control of a seed-specific (napin) promoter and the tandem 35S promoter, respectively. Seed-specific expression resulted in up to an 8-fold increase in erucic acid proportions in Arabidopsis seed oil, while constitutive expression in transgenic tobacco tissue resulted in increased proportions of very long chain saturated fatty acids. These results indicate that the nasturtium FAE gene encodes a condensing enzyme involved in the biosynthesis of very long chain fatty acids, utilizing monounsaturated and saturated acyl substrates. Given its strong and unique preference for elongating 20:1-CoA, the utility of the FAE gene product for directing or engineering increased synthesis of erucic acid is discussed.
Male Sprague-Dawley rats were fed for one week diets containing 20% by weight fat/oil mixtures with different levels of erucic acid (22:1n-9) (approximately 2.5 or 9%) and total saturated fatty acids (approximately 8 or 35%). Corn oil and high erucic acid rapeseed (HEAR) oil were fed as controls. The same hearts were evaluated histologically using oil red O staining and chemically for cardiac triacylglycerol (TAG) and 22:1n-9 content in cardiac TAG to compare the three methods for assessing lipid accumulation in rat hearts. Rats fed corn oil showed trace myocardial lipidosis by staining, and a cardiac TAG content of 3.6 mg/g wet weight in the absence of dietary 22:1n-9. An increase in dietary 22:1n-9 resulted in significantly increased myocardial lipidosis as assessed histologically and by an accumulation of 22:1n-9 in heart lipids; there was no increase in cardiac TAG except when HEAR oil was fed. An increase in saturated fatty acids showed no changes in myocardial lipid content assessed histologically, the content of cardiac TAG or the 22:1n-9 content of TAG at either 2.5 or 9% dietary 22:1n-9. The histological staining method was more significantly correlated to 22:1n-9 in cardiac TAG (r = 0.49; P less than 0.001) than to total cardiac TAG (r = 0.40; P less than 0.05). The 22:1n-9 content was highest in cardiac TAG and free fatty acids. Among the cardiac phospholipids, the highest incorporation was observed into phosphatidylserine, followed by sphingomyelin. With the addition of saturated fat, the fatty acid composition showed decreased accumulation of 22:1n-9 and increased levels of arachidonic and docosahexaenoic acids in most cardiac phospholipids, despite decreased dietary concentrations of their precursor fatty acids, linoleic and linolenic acids.
This study was undertaken to determine whether the neonate was more susceptible to the effects of dietary erucic acid (22:1n-9) than the adult. Newborn piglets were used to assess the safety of different levels of 22:1n-9 on lipid and histological changes in the heart. Newborn piglets showed no myocardial lipidosis as assessed by oil red 0 staining, but lipidosis appeared with consumption of sow milk and disappeared by seven days of age. Milk replacer diets containing soybean oil, or rapeseed oil mixtures with up to 5% 22:1n-9 in the oil, or 1.25% in the diet, gave trace myocardial lipidosis. Rapeseed oil mixtures with 7 to 42.9% 22:1n-9 showed definite myocardial lipidosis in newborn piglets, which correlated to dietary 22:1n-9, showing a maximum after one week on diet. The severity of the lipidosis was greater than observed previously with weaned pigs. There were no significant differences among diets in cardiac lipid classes except for triacylglycerol (TAG), which increased in piglets fed a rapeseed oil with 42.9% 22:1n-9. TAG showed the highest incorporation of 22:1n-9, the concentration of 22:1n-9 in TAG was similar to that present in the dietary oil. Among the cardiac phospholipids, sphingomyelin and phosphatidylserine had the highest, and diphosphatidylglycerol (DPG) the lowest level of 22:1n-9. The low content of 22:1n-9 in DPG of newborn piglets is not observed in weaned pigs and rats fed high erucic acid rapeseed oil. The relative concentration of saturated fatty acids was lowered in all cardiac phospholipids of piglets fed rapeseed oils, possibly due to the low content of saturated fatty acids in rapeseed oils. The results suggest that piglets fed up to 750 mg 22:1n-9/kg body weight/day showed no adverse nutritional or cardiac effects.
Explore the source record for details and available documents.
Normally dietary octadecapolyenoic fatty acids are anaerobically hydrogenated in ruminants, both "in vivo" in the rumen and "in vitro" with ruminal content. Here it has been investigated in artificial rumen the process concerning the erucic acid (22:1 n-9 cis) compared with and in presence of C 18 polyunsaturated acids at various incubation times. The results have shown that C 18 polyunsaturated acids hydrogenation with conversion into hydrogenation intermediates and stearic acid does always occur in contrast with erucic acid where it is never revealable, unrelated to the incubations conditions applied.