VITAMINS

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We studied the location of α-tocopherol(α-Toc) in liposome membranes, and dynamics of radical trapping and tocopherol recycling by ascorbic acid (AsA). No specific interaction was suggested to occur between the OH-group of α-Toc and the polar interfacial region of the bilayer, because of the absence of stretching bands of P = O and C = O of phosphatidylcholine by incorporation of α-Toc into liposomes, and no difference of the spin-lattice relaxation times at the 5a-position of α-Toc between positively and negatively charged liposomes. Low exposure of the chromanol at the surface of liposome membranes was supposed by little interaction with acrylamide, a water-soluble fluorescene quencher with a very low capacity to penetrate through phospholipid bilayers. Since the oxidation rate of α-Toc by positively charged Fe^<3+> was 150 times slower in negatively charged liposomes than in negatively charged SDS micelles, less than 0.65 mol% of the OH-groups of α-Toc was probably exposed at the membrane surface of liposomes. The lack of difference in the oxidation rates of α-Toc in liposomes in gel state and liquid crystalline state suggested that the OH-group was not located deeply in the hydrophobic region of membranes. Among the n-(N-oxy-4,4'-dimethyloxazolidine-2-yl) stearic acids (n-NS) labeled at different depths of membranes, 5-NS most effectively quenched the intrinsic fluorescence of α-Toc, indicating that the OH-group of α-Toc is located in a position corresponding to an inner 5-methylene carbon under the surface, where the OH-group may most efficiently trap the lipid peroxy-radicals floating up from the inner membrane core. The lipid peroxy-radicals were confirmed to float up to the membrane surface, because AsA was rapidly oxidized by 2,2'-azobis-(dimethylvaleronitrile)(AMVN), a hydrophobic radical precursor, when negatively charged AsA was ionically trapped at the positively charged surface of the liposome membranes. AsA completely suppressed the consumption of α-Toc by AMVN-induced lipid peroxidation in negatively charged liposomes. However, AsA did not penetrate into negatively charged membranes, because the ESR spectra of 5-NS and 16-NS labeled in these liposomes were not affected by the addition of AsA. These findings indicate that α-Toc is oxidized just under the membrane surface by lipid radicals, and then floats up to the surface, where it is regenerated to α-Toc by AsA.

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L-Threo-hexo-2-enaro-1,4-lactone iron (II) complex [Fe(II)-S-AsA] and its ethyl ester-iron(II) complex [Fe(II)-ES-AsA] were prepared and examined for antibacterial and antifungal actions comparatively with ascorbic acid-iron (II) complex [Fe(II)-AsA]. These iron(II) complexes showed the respective strong antibacterial actions on Enterbactor aerogenes, Bacillus subtilis, Escherichia coli, Pseudomonas aeruginosa, Staphylococcus aureus, and Bacillus cereus. [Fe(II)-S-AsA], [Fe(II)-ES-AsA] and [Fe(II)-AsA] showed antifungal action on Aspergillus niger, Geotrichum candidum, Aureobasidium pullulams, Penicillium steckii, and Trichoderma SP.

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With respect to the acute alcoholic liver injury in the mice by the administration of 86 mmol/kg of ethanol, 9.5 μmol/kg, 95 μmol/kg or 190 μmol/kg of flavin adenine dinucleotide (FAD) was administered to mice at 3 times before the administration of ethanol. The changes in the parameters, such as body weight, liver weight, flavin content, thiobarbituric acid reactive substances content and mitochondrial ADP/O ratio in the liver etc., by the administration of ethanol were dose dependently suppressed by FAD. It is suggested that an increase of lipid peroxidation and a decrease of mitochondrial ATP synthesis in the liver of mice caused by ethanol relate to the acute alcoholic liver injury. FAD shows a suppressive effect on the acute alcoholic liver injury by the decrease of lipid peroxidation and the restoration of mitochondrial ATP synthesis in the liver.

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Annual changes in polyunsaturated fatty acid (PUFA) intake per capita per day and the ratio of vitamin E to PUFA (E/PUFA) were calculated based on the data conducted from 1983 to 1988 by the National Nutrition Survey using the PUFA weighted average tables of Japanese foods, previously reported. In addition, the investigation was proposed to clarify the environmental factors on PUFA intake, (such as family members and the other environmental factors) including food habits. The people with the maximum intake of PUFAs resided in the class with three family members, in the 30 to 49 year old class, and in the class of the highest amounts of expenditure. From this survey it is verified that increase in daily intake of fats and oil, protein and energy reflected the increase in PUFA intake. The mean of the intakes of vitamin E, PUFAs and the ratio of E(mg)/PUFA(g) were 9.35±0.17 mg, 16.7±0.40 g and 0.56±0.01, respectively. Individually, the people who had undesirable balanced diet, also took either very small or large amounts of PUFA intakes.

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