Food Use and Health Effects of Soybean and Sunflower Oils

This review provides a scientific assessment of current knowledge of health effects of soybean oil (SBO) and sunflower oil (SFO). SBO and SFO both contain high levels of polyunsaturated fatty acids (PUFA) (60.8 and 69%, respectively), with a PUFA:saturated fat ratio of 4.0 for SBO and 6.4 for SFO. SFO contains 69% C18:2n-6 and less than 0.1% C18:3n-3, while SBO contains 54% C18:2n-6 and 7.2% C18:3n-3. Thus, SFO and SBO each provide adequate amounts of C18:2n-6, but of the two, SBO provides C18:3n-3 with a C18:2n-6:C18:3n-3 ratio of 7.1. Epidemiological evidence has suggested an inverse relationship between the consumption of diets high in vegetable fat and blood pressure, although clinical findings have been inconclusive. Recent dietary guidelines suggest the desirability of decreasing consumption of total and saturated fat and cholesterol, an objective that can be achieved by substituting such oils as SFO and SBO for animal fats. Such changes have consistently resulted in decreased total and low-density-lipoprotein cholesterol, which is thought to be favorable with respect to decreasing risk of cardiovascular disease. Also, decreases in high-density-lipoprotein cholesterol have raised some concern. Use of vegetable oils such as SFO and SBO increases C18:2n-6, decreases C20:4n-6, and slightly elevated C20:5n-3 and C22:6n-3 in platelets, changes that slightly inhibit platelet generation of thromboxane and ex vivo aggregation. Whether chronic use of these oils will effectively block thrombosis at sites of vascular injury, inhibit pathologic platelet vascular interactions associated with atherosclerosis, or reduce the incidence of acute vascular occlusion in the coronary or cerebral circulation is uncertain. Linoleic acid is needed for normal immune response, and essential fatty acid (EFA) deficiency impairs B and T cell-mediated responses. SBO and SFO can provide adequate linoleic acid for maintenance of the immune response. Excess linoleic acid has supported tumor growth in animals, an effect not verified by data from diverse human studies of risk, incidence, or progression of cancers of the breast and colon. Areas yet to be investigated include the differential effects of n-6- and n-3-containing oil on tumor development in humans and whether shorter-chain n-3 PUFA of plant origin such as found in SBO will modulate these actions of linoleic acid, as has been shown for the longer-chain n-3 PUFA of marine oil

Comparison of Fatty-acid Alpha-oxidation By Rat Hepatocytes and By Liver-microsomes Fortified With Nadph, Fe3+ and Phosphate

Rat liver microsomes, when fortified with NADPH, Fe3+ and phosphate, can catalyze the oxidative decarboxylation (alpha-oxidation) of 3-methyl-substituted fatty acids (phytanic and 3-methylheptadecanoic acids) at rates that equal 60-70% of those observed in isolated hepatocytes (Huang, S., Van Veldhoven, P.P., Vanhoutte, F., Parmentier, G., Eyssen, H.J., and Mannaerts, G.P., 1992, Arch. Biochem. Biophys. 296, 214-223). In the present study we set out to identify and compare the products and possible intermediates of alpha-oxidation formed in rat hepatocytes and by rat liver microsomes. In the presence of NADPH, Fe3+ and phosphate, microsomes decarboxylated not only 3-methyl fatty acids but also 2-methyl fatty acids and even straight chain fatty acids. The decarboxylation products of 3-methylheptadecanoic and palmitic acids were purified by highperformance liquid chromatography and identified by gas chromatography/mass spectrometry as 2-methylhexadecanoic and pentadecanoic acids, respectively. Inclusion in the incubation mixtures of glutathione plus glutathione peroxidase inhibited decarboxylation by more than 90%, suggesting that a 2-hydroperoxy fatty acid is formed as a possible intermediate. However, we have not yet been able to unequivocally identify this intermediate. Instead, several possible rearrangement metabolites were identified. In isolated rat hepatocytes incubated with 3-methylheptadecanoic acid, the formation of the decarboxylation product, 2-methylhexadecanoic acid, was demonstrated, but no accumulation of putative intermediates or rearrangement products was observed. Our data do not allow us to draw conclusions on whether the reconstituted microsomal system is representative of the cellular alpha-oxidation system. However, the results we obtained with [3-H-3]-labelled fatty acids indicate that during a-oxidation in intact cells the hydrogen at carbon-3, which carries the methyl branch, is not attacked

Bile-acids in Peroxisomal Disorders

We examined serum bile acids in patients with different peroxisomal disorders. Patients with Zellweger syndrome (n = 23), infantile form of Refsum disease (n = 6) and neonatal adrenoleukodystrophy (n = 4) consistently had increased levels of bile acid precursors. Patients with X-linked adrenoleukodystrophy, (n = 5) classical Refsum disease (n = 3), hyperpipecolic acidaemia (n = 4) and rhizomelic chondrodysplasia punctata (n = 9) did not have increased bile acid precursor levels. Total serum bile acids (41 micrograms ml-1) and the percentage of bile acid precursors (80%) were highest in typical Zellweger patients who died young. Long-living Zellweger patients, neonatal adrenoleukodystrophy patients and infantile Refsum disease patients had, on average, less cholestasis and a lower percentage of bile acid precursors. We also observed that total serum bile acids and the percentage of bile acid precursors decreased with age in long-living Zellweger patients. Screening for bile acid precursors, combined with very long chain fatty acids analysis is, in our experience, an easy and reliable first-line approach to the detection of peroxisomal disorder