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Five groups of salmon, of initial mean weight 127 +/- 3 g, were fed increasing levels of dietary linseed oil (LO) in a regression design. The control diet contained capelin oil (FO) only, and the same oil was blended with LO to provide the experimental diets. After an initial period of 40 wk, all groups were switched to a finishing diet containing only FO for a further 24 wk. Growth and flesh lipid contents were not affected by dietary treatment. The FA compositions of flesh total lipids were linearly correlated with dietary FA compositions (r2 = 0.88-1.00, P < 0.0001). LO included at 50% of added dietary lipids reduced flesh DHA and EPA (20:5n-3) concentrations to 65 and 58%, respectively, of the concentrations in fish fed FO. Feeding 100% LO reduced flesh DHA and EPA concentrations to 38 and 30%, respectively, of the values in fish fed FO. Differences between diet and flesh FA concentrations showed that 16:0, 18:1n-9, and especially DHA were preferentially retained in flesh, whereas 18:2n-6, 18:3n-3, and 22:1n-11 were selected against and presumably utilized for energy. In fish previously fed 50 and 100% LO, feeding a finishing diet containing FO for 16 wk restored flesh DHA and EPA concentrations, to approximately 80% of the values in fish fed FO throughout. Flesh DHA and EPA concentrations in fish fed up to 50% LO were above recommended intake values for humans for these EFA. This study suggests that LO can be used as a substitute for FO in seawater salmon feeds and that any reductions in DHA and EPA can be largely overcome with a finishing diet high in FO before harvest.
The effects of a simulated spill of sunflower oil in salt marsh sediments were compared with an experiment with linseed oil. Sunflower and linseed oil penetrated the sediments at the same rates but different adsorption of the oils onto sediment particles resulted in the establishment of anaerobic conditions at shallower depths in sediments contaminated with linseed oil than with sunflower oil. The total lipid content of sunflower oil contaminated sediments remained almost stable for 6 months, whilst only 40% of linseed oil remained in the sediment after 2 months. Numbers of culturable heterotrophic bacteria and aerobic oil degrading bacteria in muddy sediment increased rapidly in response to the presence of the oils but bacterial numbers in sandy sediments increased more slowly for sunflower oil. Changes in fatty acid composition indicate similar degradation pathways for both oils but sunflower oil degraded more slowly than linseed oil and thus has the potential for longer lasting effects in marine environments.
Effects on fatty acid profiles and milk fat yield due to dietary concentrate and supplemental 18:3n-3 were evaluated in 4 lactating Holstein cows fed a low- (35:65 concentrate:forage; L) or high- (65:35; H) concentrate diet without (LC, HC) added oil or with linseed oil (LCO, HCO) at 3% of DM. A 4 x 4 Latin square with four 4-wk periods was used. Milk yield and dry matter intake averaged 26.7 and 20.2 kg/d, respectively, across treatments. Plasma acetate and beta-hydroxybutyrate decreased, whereas glucose, nonesterified fatty acids, and leptin increased with high-concentrate diets. Milk fat percentage was lower in cows fed high-concentrate diets (2.31 vs. 3.38), resulting in decreases in yield of 11 (HC) and 42% (HCO). Reduced yields of 8:0-16:0 and cis9-18:1 fatty acids accounted for 69 and 17%, respectively, of the decrease in milk fat yield with HC vs. LC (-90 g/d), and for 26 and 33%, respectively, of the decrease with HCO vs. LCO (-400 g/d). Total trans-18:1 yield increased by 25 (HCO) and 59 (LCO) g/d with oil addition. Trans10-18:1 yield was 5-fold greater with high-concentrate diets. Trans11-18:1 increased by 13 (HCO) and 19 (LCO) g/d with oil addition. Trans13+14-18:1 yield increased by 9 (HCO) and 18 (LCO) g/d with linseed oil. Yield of total conjugated linoleic acids (CLA) in milk averaged 6 g/d with LC or HC compared with 14 g/d with LCO or HCO. Cis9,trans11-CLA yield was not affected by concentrate level but increased by 147% in response to oil. Feeding oil increased yields of trans11,cis13-, trans11,trans13-, and trans,trans-CLA, primarily with LCO. Trans10,cis12-CLA yield (average of 0.08 g/d) was not affected by treatments. Yield of trans11,cis15-18:2 was 1 g/d in cows fed LC or HC and 10 g/d with LCO or HCO. Yields of cis9,trans11-18:2, cis9,trans12-18:2, and cis9,trans13-18:2 were positively correlated (r = 0.74 to 0.94) with yields of trans11-18:1, trans12-18:1, and trans13+14-18:1, respectively. Plasma concentrations of biohydrogenation intermediates with concentrate or linseed oil level followed similar changes as those in milk fat. Milk fat depression was observed when HC induced an increase in trans10-18:1 yield. A correlation of 0.84 across 31 comparisons from 13 published studies, including the present one, was found among the increase in percentage of trans10-18:1 in milk fat and decreased milk fat yield. We observed, however, more drastic milk fat depression when HCO increased yields of total trans-18:1, trans11,cis15-18:2, trans isomers of 18:3, and reduced yields of 18:0 plus cis9-18:1.
The clinical and clinicopathologic effects of raw linseed oil and mineral oil were compared. In a crossover experimental design trial, 6 horses were given either raw linseed oil (2.5 mL/kg body weight) or mineral oil (10 mL/kg body weight), twice, 12 hours apart. Two weeks later, the horses received the opposite treatment. All horses given mineral oil or linseed oil developed nonformed feces by 24 hours of the first administration of oil. Horses treated with mineral oil had formed feces at 48 hours; horses treated with linseed oil developed normally formed feces at 96 to 108 hours. All horses treated with linseed oil had signs of depression and anorexia, and 3 had signs of mild colic. These signs were not observed in horses treated with mineral oil. Concentrations of serum glucose and bilirubin were significantly higher in horses treated with linseed oil when compared with horses treated with mineral oil.
In a short-term (15 days) experiment, weanling Wistar rats were given diets at weaning containing 10% of different linseed oils: fresh linseed oil (lot F), linseed oil heat polymerized at 275 degrees C for 12 h under nitrogen (lot T) and linseed oil oxidized in the presence of air at 200 degrees C for 100 h (lot O). We analyzed the fatty acids of total liver lipids and assayed the hydrogenated cyclic monomeric acids and identified them by using a combination of gas-liquid chromatography and mass spectrometry. Compared to lot F animals, those of lots T and O showed considerable hepatic hypertrophy but total liver lipids were not increased. However, the usual fatty acid composition of these lipids was modified: the level of several monounsaturated (16: 1, 18: 1) and polyunsaturated (mainly 20: 4n - 6) fatty acids was increased in lots T and O, which could result in increased activity of the enzymatic systems (desaturases) biosynthesizing them. Moreover, cyclic monomeric acids from heated oils were deposited at a 10 times higher concentration in the liver of lot T animals than in that of lot O animals. The significance of these changes has been discussed.
Linseed oil is an important natural sanitarian oil. To qualitative analyses the linseed oil, FTIR and FT-Raman were used to identify the contents of it. It is indicated that each component has characteristic frequency, and can be discriminated from others by IR and Raman spectroscopy. This is useful for the further on-line quantitative analysis and quality control of linseed oil.
Duodenal flows of hydrogenation intermediates in response to changes in dietary forage:concentrate ratio (F:C) and linseed oil were evaluated using 4 lactating Holstein cows fed a low (65:35 forage to concentrate) or high (35:65) concentrate diet without (LC, HC) added oil or with linseed oil (LCO, HCO) at 3% of DM. A 4 x 4 Latin square design was implemented for 5 wk. Lower hydrogenation of 18:2n-6 and 18:3n-3 was observed with HC, but it increased with LCO or HCO. Duodenal flow of total conjugated linoleic acids (CLA) increased by 1.40 (LCO) to 3.01 (HCO) g/d with linseed oil. This response was associated with greater flows of cis9,trans11- (+0.21 to +0.55 g/d), trans11,cis13- (+0.33 to +0.36), trans11,trans13- (+1.01 to +1.15 g/d), and trans,trans-CLA (+0.12 to +0.72 g/d). Trans10,cis12-CLA flow averaged 0.08 g/d and was not affected by F:C or oil. trans11,cis15-18:2 flow increased by 8.5 (LCO) to 62 (HCO) g/d in response to linseed oil. Total trans-18:1 flow was 37 g/d in cows fed LC and increased to 81 g/d with HC. Feeding oil increased total trans-18:1 to the greatest extent with HCO. Flow of trans10-18:1 was lower with LC than with HC (1.46 vs. 20 g/d). Linseed oil increased trans11-18:1 flow by 40 (LCO) to 113 g/d (HCO). Feeding LCO and HCO also increased flows of trans6+7+8-, trans13+14-, trans15-, and trans16-18:1. Apparent intestinal digestibility of trans-18:1 isomers was largely unaffected by concentrate level and ranged between 67 and 95%. Linseed oil increased digestibility of nearly all isomers by 3 to 16 percentage units. Digestibility of cis9,trans11-CLA was greater in cows fed HC (55%) compared with cows fed LC (32%) and was not affected by linseed oil. Data suggest that high concentrate diets enhanced ruminal outflow of trans10-18:1. We provide initial in vivo evidence that supplemental 18:3n-3 is hydrogenated to trans11,cis15-18:2, trans11-18:1, trans13+14-18:1, trans15-18:1, trans6+7+8-18:1, and trans16-18:1 primarily.
1. Linseed oil was incorporated gradually into the diet of four sheep until the animals received 90 g additional fat/d. Attempts were made to measure changes in concentration of substances and rates of synthesis in the rumen directly, and by incubation of rumen contents in vitro (zero-time technique). 2. The high-fat diet increased the dilution rate and the volume of rumen contents and decreased the synthesis of diaminopimelic acid in the rumen. The number of protozoa decreased and the number of bacteria increased in the rumen of animals receiving the high-fat diet. 3. The concentration of volatile fatty acids (VFA) in the rumen decreased for sheep given the high-fat diet, but the capacity of rumen contents to produce VFA in vitro increased. 4. The incorporation of radioactivity from [14C]acetate into lipids during incubation of rumen contents vitro increased with the amount of linseed oil in the diet. The greatest proportional increase was with the bacterial fraction of rumen contents. 5. In the group of four animals used, one animal showed consistent differences in the magnitude of the measured varibles. This animal appeared to have a smaller rumen, a lower dilution rate and larger concentrations of some substances in the rumen. A higher proportion of fatty acids appeared to be synthsized by the micro-organisms from this animal.
Two sequential experiments were conducted to assess the effect of replacing a fish oil diet with vegetable oil diets on broiler chicken performance and fatty acid (FA) composition and sensory traits of broiler meat. A diet enriched with 8.2% fish oil (FO) was fed to the birds throughout the 5-wk growth period (T1), the same basal diet being supplemented with 8.2% linseed oil (LO, Experiment 1) or rapeseed oil (RO, Experiment 2) in three different periods: the last week before slaughtering at 35 d (T2), the last 2 wk (T3), and throughout the experiment (T4). A sensory evaluation of the meat was carried out and its FA profile was determined. Performance parameters were not significantly different among treatments. Removing FO resulted in lower values of saturated and higher n-6 FA content, the latter because of the increase in linoleic acid in both experiments. The amounts of long-chain n-3 polyunsaturated fatty acids (PUFA) were significantly depressed when FO was replaced. However, replacing FO by LO resulted in minimal effects on total n-3 FA, due to the increase in linolenic acid. The substitution of FO by RO resulted in a decrease in the n-3 FA content, whereas levels of monounsaturated FA (MUFA) increased in direct relation to the larger amounts of oleic acid in the diet. Sensory panelists scored as unacceptable those meats from T1 in both experiments. Replacing 1 (T2) or 2 (T3) wk FO with vegetable oil clearly resulted in the improved sensory quality of meat.
The role played by membrane lipid environment on cardiac function remains poorly defined. The polyunsaturated fatty acid profile of myocardial phospholipids could be of utmost importance in the regulation of key-enzyme activities. This study was undertaken to determine whether selective incorporation of n-6 or n-3 fatty acids in membrane phospholipids might influence cardiac mechanical performances and metabolism. For 8 wk, male weaning Wistar rats were fed a semi-purified diet containing either 10% sunflower seed oil (72% C18:2 n-6) or 10% linseed oil (54% C18:3 n-3) as the sole source of lipids. The hearts were then removed and perfused according to working mode with a Krebs-Henseleit buffer containing glucose (11 mM) and insulin (10 Ul/l). Cardiac rate, coronary and aortic flows and ejection fraction were monitored after 30 min of perfusion. Myocardial metabolism was estimated by evaluating the intracellular fate of 1-14C palmitate. Sunflower seed oil and linseed oil feeding did not modify either coronary or aortic flow, which suggests that cardiac mechanical work was not affected by the diets. Conversely, cardiac rate was significantly decreased (-18%; P less than 0.01) when rats were fed the n-3 polyunsaturated fatty acid rich diet. Radioanalysis of the myocardial metabolism suggested that replacing n-6 polyunsaturated fatty acids by n-3 polyunsaturated fatty acids: i) did not alter palmitate uptake; ii) prolonged palmitate incorporation into cardiac triglycerides; iii) reduced beta-oxidation of palmitic acid. These results support the assumption that dietary fatty acids, particularly n-6 and n-3 fatty acids, play an important role in the regulation of cardiac mechanical and metabolic activity.
In male C3H/He mice, which frequently develop spontaneous liver tumorigenesis, 5 wk of age and weighing about 20 g, the comparative effects on liver tumor incidence from the feeding of olive oil (OLI), safflower oil (SAF), and linseed oil (LIS) diets for 50 wk, the concentrations of total cholesterol (T-CHOL), triacylglycerol (TG), lipid peroxides in the plasma and liver, and the activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in the plasma were examined. The changes in body weight and liver weight were not different among dietary groups. The number of mice bearing liver adenoma was greater in the SAF group than in the OLI and LIS groups. Liver carcinoma was observed in the SAF group, but not in the OLI and LIS groups. The concentrations of T-CHOL in the plasma and liver were higher in the OLI group than in the other groups. TG levels in the plasma and liver were highest in the OLI group and followed in order by the SAF and LIS groups. The concentration of plasma lipid peroxide was higher in the LIS group than in the other groups. Liver lipid peroxide content was extremely high in the LIS group, medium in the SAF group, and low in the OLI group. The activity of AST was highest in the OLI group and followed in order by the SAF and LIS groups. ALT activity was higher in the OLI group than in the other groups. A positive relationship between spontaneous liver tumorigenesis and the concentrations of T-CHOL, TG, and lipid peroxide or AST and ALT activities was hardly observed. These results suggested that spontaneous tumorigenesis in the liver of male C3H/He mice bred for 50 wk was suppressed by being supplied with OLI and LIS, compared with SAF, which had no direct relation to the concentrations of T-CHOL, TG, and lipid peroxide in the plasma and liver and the activities of plasma AST and ALT.
In a simulated spill in a salt marsh, linseed oil penetrated rapidly into the sediments at a rate of 10(-7) cm2 s(-1). The oil concentration remained unchanged for the first month after the spill, but 60% of the oil disappeared from the top 30 cm after a further month. The oil adsorbed to and accumulated in the muddy sediments (top 15 cm) leading to decreased sediment permeability, pH, Eh, abundance of plant roots and infauna and to the establishment of anoxic conditions. These changes accompanied transformations in the original fatty acid composition of the linseed oil, mainly associated with a decrease in 18 : 3omega3, an increase in the other fatty acids and the presence of 'new' fatty acids. A rapid increase in the abundance of heterotrophic aerobic and anaerobic bacteria and aerobic oil degrading bacteria, suggested that these micro-organisms degraded the oil. The role of the bacteria in oil degradation was confirmed in laboratory experiments where the fatty acids composition of the linseed oil underwent identical transformations to those obtained in the field. The degradation of linseed oil appears to be a sequential process initiated by aerobic and/or anaerobic bacteria and continued by sulphate reducing bacteria, which were unable to degrade the raw oil.
Endotoxin stimulates macrophages to synthesize membrane-associated inflammatory mediators including eicosanoids and procoagulant activity (PCA). Alpha linolenic acid, a component of linseed oil, is metabolized to eicosapentaenoic acid, which may replace arachidonic acid in membrane phospholipids. Thus, ingestion of linseed oil may alter the generation of eicosanoids, PCA and other membrane-dependent responses. This study compared the in vitro endotoxin-induced synthesis of eicosanoids and expression of PCA by peritoneal macrophages obtained from rats fed a control diet and rats fed a diet enriched with linseed oil. The effect of endotoxin on in vivo plasma eicosanoid concentrations, leukogram, and microvascular permeability were determined. Endotoxin (5 ug/ml) stimulated synthesis of iTxB2, i6-keto PGF1 alpha and expression of PCA by macrophages in vitro. These in vitro responses of macrophages from linseed oil fed rats were significantly less than those of macrophages from control rats. In contrast, there were no significant differences in in vivo responses to endotoxin. The fatty acid composition of total lipids and phospholipids in liver and plasma from linseed oil fed rats and control rats were not different. These composite data suggest several possibilities: (1) linseed oil may have effects independent of alpha-linolenic acid on macrophage function, (2) linseed oil may alter the fatty acid composition of macrophage phospholipids prior to changing that of other tissues, and (3) the reduced in vitro responses of peritoneal macrophages may not reflect the systemic responses to endotoxin.
Four groups of rabbits were studied to determine the effect of linseed oil on cholesterol-induced atherosclerosis. Group C received cholesterol alone; group CL received cholesterol and linseed oil, group L were given linseed oil alone, while group N were fed the normal stock diet for 18 weeks. Cholesterolemia was marked in groups C and CL but not in groups L or N. Cholesterolemia was significantly greater (P less than 0.001) in group CL (462 mg/dl) than in group C (318.6 mg/dl). Thus, the addition of linseed oil to cholesterol led to greater hypercholesterolemia than with the cholesterol diet alone. There was no significant change in the serum triglyceride level in either group. Atherosclerotic lesions (mostly fatty streaks but some fibrous plaques) were present only in groups C and CL and were absent in groups L and N. The percentage of atherosclerotic intimal involvement was significantly greater in group CL than C (P less than 0.001). The severity of atherosclerosis correlated with serum cholesterol levels (r = 0.79, P less than 0.001), but not with serum triglyceride levels.
Only few informations exist on the effect of different oils and the transformation of these precursor fatty acids to prostaglandins in patients with hyperlipoproteinemia. Therefore we investigated the impact of linseed oil and olive oil intake resp. on serum lipoprotein levels, platelet aggregation and fatty acid pattern of serum phospholipids and triglycerides resp. in patients with primary hypercholesterolemia (HC) (n = 13) and hypertriglyceridemia (HTG) (n = 16). The probands were randomly admitted to a 4 week test period with 30 ml olive or linseed oil intake. After linseed or olive oil intake all lipid fractions did not change significantly. Olive oil significantly reduced the platelet aggregation only in patients with HTG, whereas linseed oil failed to influence aggregation. After linseed oil intake there was a significant increase in linolenic and also in eicosapentaenoic acid content of phospholipids in patients with HTG. In contrast to HTG in HC linseed oil only increased significantly the linolenic acid fraction. Our data suggest, that the response of serum lipoproteins, fatty acids and platelet aggregation on modifications in dietary fats depends on the type of lipoprotein disorder.
Ten healthy volunteers daily received 30 ml linseed oil for 4 weeks in addition to the "normal" diet. The influence of linseed oil diet on the fatty acid pattern of plasma phospholipids and thromboxane formation in platelets was investigated. The fatty acid pattern was analysed by gas liquid chromatography. The alpha-linolenic, eicosapentaenoic and docosahexaenoic acids were increased (p less than 0.01), whereas linoleic and arachidonic acids were decreased (p less than 0.05) after 4 weeks of the linseed oil diet. The thromboxane formation of platelets were unchanged. Additionally the influence of HDL and LDL on PGI2 biosynthesis in pig aortic microsomes (PAM) was investigated. HDL taken from serum before and after 3 weeks of linseed oil diet and LDL taken after 3 weeks of diet stimulated the PGI2 formation in PAM, whereas LDL taken from serum before the diet period inhibited the PGI2 formation in PAM.
Syntheses of wholly natural polymeric linseed oil (PLO) containing peroxide groups have been reported. Peroxidation, epoxidation and/or perepoxidation reactions of linseed oil, either under air or under oxygen flow at room temperature, resulted in polymeric peroxides, PLO-air and PLO-ofl, containing 1.3 and 3.5 wt.-% of peroxide, with molecular weights of 2 100 and 3 780 Da, respectively. PLO-air contained cross-linked film up to 46.1 wt.-% after a reaction time of 60 d, associated with a waxy, soluble part (PLO-air-s) that was isolated with chloroform extraction. PLO-ofl was obtained as a waxy, viscous liquid without any cross-linked part at the end of 24 d under visible irradiation and oxygen flow. Polymeric peroxides, PLO-air-s and PLO-ofl initiated the free radical polymerization of both methyl methacrylate (MMA) and styrene (S) to give PMMA-graft-PLO and PS-graft-PLO graft copolymers in high yields with Mw varying from 37 to 470 kDa. The polymers obtained were characterized by FT-IR, (1)H NMR, TGA, DSC and GPC techniques. Cross-linked polymers were also studied by means of swelling measurements. PMMA-graft-PLO graft copolymer film samples were also used in cell-culture studies. Fibroblast cells were well adhered and proliferated on the copolymer film surfaces, which is important in tissue engineering.