Consumption Of Rapeseed Oil Research Articles

Dietarytrans α-linolenic acid does not inhibit Δ5- and Δ6-desaturation of linoleic acid in man

Dietary trans monoenes have been associated with an increased risk of heart disease in some studies and this has caused much concern. Trans polyenes are also present in the diet, for example, trans α-linolenic acid is formed during the deodorisation of α-linolenic acid-rich oils such as rapeseed oil. One would expect the intake of trans α-linolenic acid to be on the increase since the consumption of rapeseed oil in the western diet is increasing. There are no data on trans α-linolenic acid consumption and its effects. We therefore carried out a comprehensive study to examine whether trans isomers of this polyunsaturated fatty acid increased the risk of coronary heart disease. Since inhibition of A6-desaturase had also been linked to heart disease, the effect of trans α-linolenic acid on the conversion of [U- 13 C]-labelled linoleic acid to dihomo-γ-linolenic and arachidonic acid was studied in 7 healthy men recruited from the staff and students of the University of Edinburgh. Thirty percent of the habitual fat was replaced using a trans free'- or 'high' trans α-linolenic acid fat. After at least 6 weeks on the experimental diets, the men received 3-oleyl, 1,2-[U- 13 C]-linoleyl glycerol (15 mg twice daily for ten days). The fatty acid composition of plasma phospholipids and the incorporation of 13 C-label into n-6 fatty acids were determined at day 8, 9 and 10 and after a 6-week washout period by gas chromatography-combustion-isotope ratio mass spectrometry. Trans α-linolenic acid of plasma phospholipids increased from 0.04 ± 0.01 to 0.17 ± 0.02 and cis α-linolenic acid decreased from 0.42 ± 0.07 to 0.29 ± 0.08 g/100 g of fatty acids on the high trans diet. The composition of the other plasma phospholipid fatty acids did not change. The enrichment of phosphatidyl 13 C-linoleic acid reached a plateau at day 10 and the average of the last 3 days did not differ between the low and high trans period. Both dihomo-γ-linolenic and arachidonic acid in phospholipids were enriched in 13 C, both in absolute and relative terms (with respect to 13 C-linoleic acid). The enrichment was slightly and significantly higher during the high trans period (P L'effet d'un regime alimentaire enrichi en acide trans α-linolenique, du par exemple a l'augmentation de la consommation d'huile de colza, a ete etudie chez 7 hommes volontaires et sains, le but etant de demontrer si la consommation accrue de l'isomere trans de cet acide gras polyinsature augmente le risque de cardiopathie coronaire. Comme l'inhibition de l'enzyme Δ6-desaturase a egalement ete liee a ce risque cardiovasculaire, l'effet de l'acide trans α-linolenique sur la conversion de l'acide linoleique en dihomo-γ-linolenique et acide arachidonique a ete etudie, en dosant la composition en acide gras des phospholipides plasmatiques. Les resultats suggerent que ce regime alimentaire riche en acide trans α-linolenique n'inhibe pas la conversion de l'acide linoleique.

Characteristics of denatured rapeseed oil during storage and refining processes

In 1981, toxic oil syndrome, a progressive multi-system disease caused by consumption of rapeseed oil denatured with aniline occurred in Spain. To date, the causal toxic agent or agents remain unknown. Measures of acidity, moisture, impurities, phosphorous, soaps, and spectrophotometric determinations of color at 409 nm were performed. Since fatty acid anilide concentrations in these oils are associated with risk of disease, w e studied the formation of aniline-derived compounds over time after oil denaturation and by oil deodorization temperatures (200oC, 215oC, 230oC, 245oC, 260oC, y 270oC) and times (3, 4, 4.5, 5, 5.5 and 6 hours). Formation of fatty acid anilide compounds increased with storage time. Deodorization led to a reduction of total anilides in all the samples, particularly at temperatures above 245oC. Esters of 3-(N-phenylamino)-1,2-propanediol were not detected.

Epidemiologic Evidence for a New Class of Compounds Associated with Toxic Oil Syndrome

Toxic oil syndrome appeared in epidemic form in Spain in 1981. Epidemiologic studies have demonstrated that illness was caused by consumption of rapeseed oil that had been denatured with aniline. Chemical analyses of oil specimens conducted in conjunction with epidemiologic studies have established that consumption of specific oils containing fatty acid anilide contaminants was associated with increased risk for disease. New chemical analytic methods identified a family of compounds, the di-fatty acid esters of phenylamino propane-diol, and one of these compounds, the 1,2-di-oleyl ester of 3-(N-phenylamino)-1,2-propanediol (DPAP), has been found to be more strongly associated with disease status than the fatty acid anilides. We found the odds ratio for exposure to DPAP (OR = 26.4, 95% CI = 6.4-76.3) is much higher than the odds ratio for exposure to oleyl anilide (OR = 4.1, 95% CI = 2.2-7.8), implying that exposure to DPAP was a more relevant risk factor for development of toxic oil syndrome than exposure to oleyl anilide. In this paper, we review and present analyses of data from multiple studies of the possible etiologic role of DPAP in toxic oil syndrome. The presence of DPAP in oil collected from affected and unaffected households was a more specific correlate of case relatedness than was the presence of fatty acid anilides, and it was equally sensitive. Moreover, DPAP was found in oil from the only refinery whose oil was clearly associated with illness.

Change of mycelial morphology in tylosin production by batch culture of Streptomyces fradiae under various shear conditions

Morphological change during culture of the tylosin producer Streptomyces fradiae under various shear conditions was investigated using an image analysis system. The morphology was classified as filament, entangled filament, or pellet by measuring the mycelial area and convex perimeter. At fermentor agitation rates of 400 rpm and higher, filament and entangled filament morphology comprised more than 50%. However, in cultures at agitation rates lower than 400 rpm, pellet morphology increased gradually and until it comprised more than 50%; in an air-lift reactor, the pellet ratio reached 80% after 160-h culture. The average areas of pellets and mycelia in the air-lift reactor were respectively 100- and 20-fold those under high shear condition. Both pellet area and mycelial morphology changed during the culture period according to the shear conditions. Among the various shear conditions, tylosin production and rapeseed oil consumption were lowest in the airlift fermentor culture with against in the fermentor at 400 rpm. From the viewpoint of tylosin production, the optimal mycelial area that gave the maximum production rate under various shear conditions was around 4 × 10 3 μm 2. When the mycelia and pellet areas exceeded 4 × 10 3 μm 2, the tylosin production rate decreased drastically.

Autoantibodies to cryptic epitopes of C-reactive protein and other acute phase proteins in the toxic oil syndrome.

Toxic oil syndrome (TOS) was caused by the consumption of rapeseed oil contaminated with derivatives of aniline. Many persons who survived the acute phase developed a puzzling, multi-year chronic disease considered to be inflammatory or autoimmune in nature. In attempting to characterize their autoantibodies, we found that 74% of TOS patients with chronic disease had IgG antibodies to C-reactive protein (CRP). This activity was detectable only when CRP was chemically or physically denatured and behaved like a previously described antibody produced by immunization with the CRP monomer. Significant antibody reactivities to other acute phase proteins, especially alpha 1-antitrypsin and fibrinogen (P < 0.025) and ceruloplasmin (P < 0.05) were also observed. IgG antibodies to cryptic epitopes in CRP and other major serum proteins that increase during the acute phase response may reflect an earlier toxin-mediated insult to the liver that included abnormal biosynthesis of and/or damage to acute phase proteins.

Effects of a monounsaturated rapeseed oil and a polyunsaturated sunflower oil diet on lipoprotein levels in humans.

The effects of high oleic acid rapeseed oil compared with polyunsaturated fats on serum lipoprotein levels are largely unknown. Therefore, we fed 30 women and 29 men a baseline diet rich in saturated fat, which was followed by a diet rich in high oleic and low erucic acid rapeseed oil (total energy content of fat, 38%; saturates, 12.4%; monounsaturates, 16%; n-6 polyunsaturates, 6%; and n-3 polyunsaturates, 2%) and one rich in sunflower oil (total energy content of fat, 38%; saturates, 12.7%; monounsaturates, 10%; n-6 polyunsaturates, 13%; and n-3 polyunsaturates, 0%). The oils were incorporated into mixed natural diets that were dispensed in a random order for 3.5 weeks each in a blinded crossover design. The diet composition was confirmed by analysis of duplicate diets. Both test diets reduced serum total cholesterol (TC) and low density lipoprotein (LDL) cholesterol levels from baseline, the monounsaturated rapeseed oil diet more than the polyunsaturated sunflower oil diet (TC: -15% versus -12%, p less than 0.01; LDL cholesterol: -23% versus -17%, p less than 0.01). Very low density lipoprotein (VLDL) cholesterol and total, VLDL, and LDL triglyceride levels were lower during the sunflower oil diet compared with the rapeseed oil diet. Total high density lipoprotein (HDL) cholesterol levels remained unchanged by both diets. The consumption of rapeseed oil resulted in a more favorable HDL2 to LDL cholesterol ratio (0.43 +/- 0.19 versus 0.39 +/- 0.18, p less than 0.01) and an apolipoprotein A-I to B ratio (3.0 +/- 1.4 versus 2.4 +/- 1.6, p less than 0.001) than did the sunflower oil.(ABSTRACT TRUNCATED AT 250 WORDS)

Manufacturing processes at two French rapeseed oil companies: Possible relationships to toxic oil syndrome in Spain

The toxic oil syndrome (TOS) epidemic that occurred in Spain in spring 1981 has been associated with the consumption of rapeseed oil that was denatured with aniline for industrial use but diverted for human consumption. The precise aetiologic agent in the oil responsible for the outbreak has not been identified. To learn more about possible contaminants and how the contamination might have occurred, we visited two French companies that process rapeseed oil and that were identified in Spanish administrative and judicial records as the ones exporting aniline-denatured rapeseed oil to Spain in 1981. With the apparently full and voluntary co-operation of personnel at both companies, we reviewed the processes involved in manufacturing, treating and transporting rapeseed oil, and we have summarized the information provided to us. Of particular importance is the finding that oil exported to Spain was taken from stock, the rest of which was sold for human consumption in the French domestic market, apparently without any adverse health effects. The differences between the oil exported to Spain and the oil sold as food in France were that aniline equivalent to 2% of the weight of the oil was added to most of the Spanish oil but not to that sold in France, and that contamination of the Spanish oil may have occurred in the tank trucks used for transportation to Spain, which had previously carried industrial chemicals. There is no assurance that the trucks were cleaned appropriately for transporting a food product before the oil was loaded for the journey to Spain. Since the clinical manifestations of TOS are not those of aniline toxicity, we conclude that the aetiological agent of TOS is likely to be one of the following: (1) a contaminant in the aniline, (2) a contaminant introduced during transportation, (3) a reaction product of normal oil components or materials used in refining with either aniline or the potential contaminants mentioned under (1) or (2) above.

Erucic acid metabolism by rat heart preparations.

Rat heart preparations metabolized erucic acid at much slower rates than palmitic acid. This applied for activation reaction, for the conversion of acyl-CoA to acylcarnitine, and for the utilization of acyl group for oxidation. As compared to palmityl-CoA, erucyl-CoA exhibited a lower affinity for carnitine palmityltransferase (EC 2.3.1.23), the respective apparent Michaelis constants were 43 and 83 muM. Presence of erucyl-CoA or erucyl-carnitine slowed the mitochondrial oxidation of palmityl groups apparently because of the slower oxidation of erucyl groups. However, presence of erucate did not inhibit the activation of palmitate. Heart mitochondria obtained from rats fed rapeseed oil (50 cal %) or corn oil diet for 3 days showed similar abilities for the coupled oxidation of various substrates and similar carnitine palmityltransferase activities. Thus, a suggestion of gross mitochondrial malfunction following rapeseed oil consumption was not confirmed.