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Results for “Cod Liver Oil”

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At least 541 records · Page 30Linked to original sources
PubMed1992

Inhibition of phenytoin bioactivation and teratogenicity by dietary n-3 fatty acids in mice.

Evidence suggests that the teratogenicity of the anticonvulsant drug phenytoin (DPH) can result from its bioactivation via embryonic prostaglandin synthase and/or maternal cytochromes P450. This study examined whether DPH bioactivation and teratogenicity could be reduced by dietary n-3 fatty acids. Female CD-1 mice were fed diets containing 2 wt% safflower oil and 10 wt% of either hydrogenated coconut oil, safflower oil, or a cod liver oil/linseed oil mixture (CLO/LO) for three weeks prior to impregnation and throughout gestation. DPH (55 or 65 mg/kg) was administered via intraperitoneal injections to pregnant mice at 0900 on gestational days 12 and 13, and on day 19 fetuses were given teratologic assessments. A similar dietary study evaluated in vivo covalent binding of radiolabeled DPH administered on day 12, and dams were killed 24 h later. A reduction in DPH-induced cleft palates and a decrease in DPH covalent binding to embryonic protein was observed in the CLO/LO group. Feeding CLO/LO enhanced incorporation of n-3 fatty acids into embryos and inhibited embryonic prostaglandin synthase activity. No differences in maternal hepatic cytochromes P450 activities were observed among dietary treatments. These data indicate that dietary n-3 fatty acids could reduce DPH teratogenicity via inhibition of embryonic prostaglandin synthase bioactivation of DPH.

Abnormalities, Drug-Induced↗
PubMed2001

Delayed-type hypersensitivity and humoral immunity modulation by dietary lipids in a murine model of pulmonary tumorigenesis induced by urethan.

Mice fed on semisynthetic formulas containing 15% of corn oil (CO), cod fish liver oil (FO), oleic acid (O) or a mixture of 46% of palmitic and 50% of stearic acids (PS) were treated with urethan during 18 weeks for lung tumor induction. Delayed-type hypersensitivity (DTH) assay, hemagglutination assay and the amount of lung nodes (alveolar adenocarcinomas) were recorded. Results showed significantly greater DTH in CO and FO with respect to O and PS feeding mice; the two last ones induced an essential fatty acid (EFA) deficiency (EFAD). In the O lot there was a non-significant diminution of the humoral response. EFAD animals exhibited a tendency to increase number of lung nodes in relation to CO and FO lots. Splenomegalia was recorded in FO lot. Confront between spleen weight and DTH showed a 72% correlation, suggesting an increase in cellular immunity as increasing unsaturation. It may be concluded that in this suitable model of tumorigenesis the manipulation of dietary lipids may be a strategy to modify the immune system response.

Adenocarcinoma↗
PubMed1989

n-3 fatty acid deficiency in man.

A total of nine patients with n-3 fatty acid deficiency are described. They had been fed by gastric tube for 2.5-12 years, and had received 0.02-0.09% of calories as n-3 acids. The observed clinical symptoms of n-3 fatty acid deficiency were scaly and haemorrhagic dermatitis, haemorrhagic folliculitis of the scalp, growth retardation and impaired wound healing. All patients had extensive brain damage making it impossible to evaluate n-3 effects on cerebral functions. The patients were supplemented with cod liver and soya oil, alpha-linolenate followed by a purified fish oil, or with a mixture of linseed and cod liver oil. The results indicate that a dietary supply of 1.0-1.2% of alpha-linolenic acid is necessary to obtain a mid-normal lipid concentration of n-3 fatty acids, and suggest that the minimal dietary requirement is 0.2-0.3% of total calories. Long-chain n-3 fatty acids seem to be approximately twice as efficient as alpha-linolenic acid in maintaining normal n-3 fatty acid concentrations in plasma and red cell lipids.

Aged↗
PubMed1989

Physico-chemical properties of cholesterol-fed rabbit beta-VLDL are not affected by different dietary oils.

Various oils have been used as vehicles for cholesterol in diets used to produce atherosclerosis in rabbits. Because such oils may affect the physico-chemical properties of the beta-VLDL produced in response to cholesterol feeding, we have studied the physico-chemical characteristics of beta-VLDL isolated from cholesterol-fed rabbits using several different oils as vehicles (corn, safflower, cod liver, and peanut oils). All animals developed severe hypercholesterolemia by 2 weeks. During the second and third weeks on diet the apo beta-containing lipoproteins began to develop thermal transitions due to order-disorder cholesterol ester transitions in the lipoproteins. By 4 weeks the apo beta-containing lipoproteins (overwhelmingly beta-VLDL) had transitions which were quite similar (transition temperatures 41.0-42.5 degrees C). No statistical differences were noted between the transition temperatures or enthalpies of any of the dietary groups. Thus, the physico-chemical properties of the beta-VLDL of rabbits fed cholesterol appear to be quite similar, despite the vehicles used to carry the cholesterol in the diet. Thus other mechanisms must be looked for to explain the different atherogenicity of different oils used as cholesterol carrying vehicles.

Animals↗
PubMed1977

Lack of fatty acid specificity in the lipolysis of oligo and polyunsaturated triacylglycerols by milk lipoprotein lipase.

Native soybean and rapeseed oils and native and rearranged cod liver and peanut oils were subjected to partial hydrolysis with milk lipoprotein lipase and the fatty acid composition and molecular association in the substrates and lipolysis products were determined. In both native and rearranged oils the lack of significant differences in the fatty acid composition and molecular association between the residual and total triacylglycerols suggested that all triacylglycerols were attacked by the lipoprotein lipase at about the same rate. Any enrichment of a specific fatty acid in the diacyl- or monoacylglycerol products of a native oil generally reflected the preferential association of the fatty acid with the 2-position, and to a lesser extent the sn-3-position of the glycerol molecule and was accompanied by a decreased level of the corresponding free fatty acid product. In general, the products of the rearranged oils closely resembled the original triacylglycerols in the fatty acid composition. It is concluded that lipoprotein lipase does not show any detectable specificity for the unsaturated and polyunsaturated fatty acids with double bonds located at carbons 3 to 19 from the carboxyl end of the fatty acid molecules. These findings are compatible with the possible binding of the substrate to lipoprotein lipase through atoms involved in the acyl ester groups of the triacylglycerol molecules.

Animals↗