The variation in fatty acid composition between the "bound" and "free" lipid in stored anchovy meal was determined using gas-liquid chromatographic analysis. A model system of fresh anchovy oil on powdered lactalbumin was also studied to determine the changes in extractability and fatty acid composition which occur during oxidation. All of the lipid-protein systems examined were first extracted with hexane. The extracted protein was then extracted with choroform:: methanol (2:1 v/v), and finally digested in HCl and the hydrolysate extracted with diethyl ether. The chloroform : methanol extract and HCl digestion represented oil which was bound to the protein. Each lipid extract was interesterified with methanol to yield the corresponding methyl esters, and these esters were then analyzed by gas-liquid chromatography. Both quantitative and qualitative analysis was carried out using a diethylene glycol succinate packed column in a gas chromatograph equipped with a hydrogen flame detector. The results of these investigations showed that the oil from anchovy meal differed markedly in fatty acid composition from the corresponding fresh oil. Although the types of fatty acids found were identical to those in the fresh oil, there was considerable quantitative variation. These differences were characterized by smaller amounts of polyunsaturated fatty acids in the meal, and correspondingly larger amounts of saturated and monoenoic fatty acids. The greatest change occurred in the acid, 20:5. Anchovy meal contained a "bound" lipid fraction which varied in quantitative fatty acid composition with the readily extractable lipid. The fractions associated with the protein had higher proportions of 22:4, 22:5, and 22:6, with the acid digest fraction considerably lower in the monoenoic fatty acids. The oxidation of anchovy oil and anchovy oil methyl esters on lactalbumin produced a reduction in hexane extractable lipid with a corresponding increase in lipid which was soluble only in chloroform : methanol or after HCl hydrolysis. These changes were more drastic when untreated anchovy oil was used. The oxidation of anchovy oil methyl esters on lactalbumin produced a reduction in the amounts of polyunsaturated fatty acids present in the hexane extract. The other solvent extractions, however, yielded only higher molecular weight compounds which could not be analyzed by GLC. These observations led to the conclusion that the fatty acids formed compounds which interacted before being bound to the protein. / Graduation date: 1966

Graduation date: 1991

Thesis (M.S.)--University of Hawaii at Manoa, 2007. / Includes bibliographical references (leaves 46-54). / x, 54 leaves, bound ill. 29 cm

The physicochemical characteristics of seven cold-pressed flaxseed oils sold in New Zealand were investigated for their fatty acid composition, tocopherol composition, moisture and volatile matter, free fatty acids, chlorophyll pigments, unsaponifiable matter, total phenolic acids and flavanoids, and colour. The seven cold-pressed flaxseed oils exhibited significant variations in their physicochemical characteristics. Quality of the oils in terms of oxidative stability was also investigated. Four oils were found to be within the limit of good stability oil indices, measured in terms of peroxide value, p-anisidine value, conjugated dienoic acids, specific extinction in ultraviolet spectrum, acid value and food oil sensor readings (to indicate total polar compounds). The role of minor constituents in the oxidative stability of two selected oils with different levels of fatty acid composition and minor constituents was investigated. Pan heating at 150�C caused loss of tocopherols, plastochromanol-8, phenolic acids, chlorophyll pigments, β-carotene and lutein and changes in the fatty acid composition. The pan-heated oils exceeded the limit of good stability oil indices using the measurement mentioned above except for acid value. The addition of α-tocopherol to the oils did not provide enhanced protection to the oils in accelerated aging of oil tests at 60�C. It was most likely that phenolic acids present in the oils played a dominant role in the oxidative stability of the oils. Lipase-catalyzed transesterification of triolein with cinnamic and ferulic acids using a commercially available immobilized lipase B from Candida antarctica (Novozym 435) was conducted to evaluate the antioxidant activity of the lipophilized products as model systems for enhanced protection of unsaturated oil. The lipophilized products were identified using Electrospray Ionization-Mass Spectroscopy (ESI-MS). Separation and isolation of two classes of lipophilized products was also achieved using a solid phase extraction method developed in this study for further investigation into the structure-free radical scavenging activity. Free radical scavenging activity was determined using the 2,2-diphenyl-1-picrylhydrazyl radical (DPPH) method. The polarity of the solvents proved important in determining the free radical scavenging activity of the substrates. Ferulic acid showed much higher free radical scavenging activity than cinnamic acid, which had limited activity. The esterification of cinnamic acid and ferulic acid with triolein resulted in significant increase and decrease in the free radical scavenging activity, respectively. These opposite effects were due to the effect of addition of electron-donating alkyl groups on the predominant mechanism of reaction (hydrogen atom transfer or electron transfer) of a species with DPPH. The effect of esterification of cinnamic acid was confirmed using ethyl cinnamate which greatly enhances the free radical scavenging activity. Although, compared with the lipophilized cinnamic acid product, the activity was lower. The free radical scavenging activity of the main component isolated from lipophilized cinnamic acid product using solid phase extraction, monocinnamoyldioleoylglycerol, was as good as the unseparated mixture of lipophilized product. Based on the ratio of a substrate to DPPH concentration, lipophilized ferulic acid was a much more efficient free radical scavenger than lipophilized cinnamic acid. Lipase-catalyzed transesterification of flaxseed oil with cinnamic and ferulic acids using Novozym 435 was conducted to evaluate whether the lipophilized products provided enhanced antioxidant activity in the oil. The lipophilized products were identified using ESI-MS and were examined for their free radical scavenging activity toward DPPH in ethanol and ethyl acetate. Ferulic acid showed the highest free radical scavenging activity among all substrates tested while cinnamic acid had negligible activity. The effect of esterification of cinnamic acid and ferulic acid with flaxseed oil was similar to that with triolein. Lipophilized ferulic acid was a better free radical scavenger as compared with lipophilized cinnamic acid and extended the naturally-occuring antioxidant capacity of the flaxseed oil. Lipophilized cinnamic acid did not provide much enhanced radical scavenging activity in the flaxseed oil as the presence of natural hydrophilic antioxidants in the oil had much greater radical scavenging activity. It may still be useful for unsaturated oils with a small amount of natural antioxidants in them. Lipophilized cinnamic and ferulic acids showed higher free radical scavenging activity when tested in a less polar solvent (ethyl acetate) whereas ferulic acid showed better activity in a more polar solvent (ethanol). These results indicate that the choice of solvent for the DPPH assay is critical in evaluating the free radical scavenging activity of substrates of differing polarity, and support previous observations by other authors that the solubility of an antioxidant in relation to the site of oxidation is an important factor for consideration in the use of antioxidants.

Title page, summary and table of contents only. The complete thesis in print form is available from the University of Adelaide Library. / Tumor necrosis factor (TNF) is a pro-inflammatory cytokine with multiple biological effects. The receptors for this cytokine on neutrophils have been shown to be rapidly down-regulated following activation, leading to the release of soluble forms of these receptors. Thus neutrophils become less responsive to TNF and the soluble TNF receptors (TNFR) serve to control TNF activity. During inflammation, leukocytes become activated as a result of the action of a variety of mediators. These mediators include not only cytokines but also lipids, such as the pro-inflammatory 00-6 fatty acid, arachidonic acid (AA) and its metabolites. Cellular activation leads to the release of AA from membrane phospholipids. AA regulates the function of many cell types including neutrophils. In view of the known pro-inflammatory properties of AA and the anti-inflammatory properties of 00-3 fatty acids, a study was undertaken to examine whether or not these fatty acids regulate the expression and release of TNFR in neutrophils. While much emphasis has been placed on agonist-induced down-regulation of TNFR, our data show that AA causes a rapid (10-20 min) and dose-dependent (0.5 to 30 uM) increase (8-fold) in the surface expression of both classes of TNFR (TNFRl and TNFRlI) on human neutrophils, at concentrations found in inflammatory fluids. This correlates with an increase in superoxide production to a TNF challenge. In contrast, both fMLP and LPS significantly reduce the expression of both TNF receptors. Interestingly, in neutrophils pretreated with AA, fMLP causes an increase in TNF receptor expression, consistent with AA preventing the fMLP-induced receptor release in neutrophil culture. In addition, while AA causes an increase in TNF receptor expression on matured HL-60 cells (neutrophil-like cells), a decrease occurs on HUVEC and non-matured HL-60 cells. These data demonstrate a unique effect of AA on neutrophils. The relationship between AA and the anti-inflammatory (0-3 fatty acids, DHA and eicosapentaenoic acid (EPA), in the modulation of TNF receptor expression has also been examined. These (0-3 polyunsaturated fatty acids, including linolenic acid (LNA), cause a decrease in TNFR expression on neutrophils. The (0-6 linoleic acid (LA) and (0-9 oleic acid (OA) both cause an increase in TNFR expression. Furthermore, pre-exposure of neutrophils to nanomolar amounts of EPA or DHA prevents the AA-induced up-regulation of TNFR. These results thus identify another mechanism of regulating the inflammatory reaction by the (0-3 fatty acids. The mechanisms by which AA induces an increase in TNFR expression have been studied. Masking of the carboxyl group results in loss of activity. It is unlikely that a product of AA is responsible since neither the hydroperoxyeicosatetraenoic acid, nor hydroxyeicosatetraenoic acid derivatives show activity. Also, the effects of AA are not sensitive to the action of inhibitors of the cyclooxygenases and lipoxygenases. Using chemical inhibitors of intracellular signaling pathways, we demonstrate that the effect of AA on TNFRI is very sensitive to GFI09203X, PD098059, AACOCF3 and wortmannin, showing a role for protein kinase C, the extracellular signal regulated protein kinases and cytoplasmic phospholipase A2, and PI-3 kinase respectively, in the enhancement of TNF receptor expression by AA. Although the effects of AA on TNFRII are also decreased by the chemical inhibitors, the results show that these signalling molecules only contribute in part to the mechanisms of increased TNFRII receptor expression. The data presented in this thesis suggest a novel role for AA in the inflammatory reaction, through its action on neutrophil TNFR expression. The work has identified a unique effect of 00-3 polyunsaturated fatty acids for regulating this AA-induced increase in the expression of TNF receptors. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1141955 / Thesis (Ph.D.) -- University of Adelaide, Dept. of Paediatrics, 2004

Thesis (M. Res.(Med.))--University of Hong Kong, 2007.

Thesis (Ph.D.) -- McMaster University, 1999. / (Alpha) in title is a Greek letter. Includes bibliographical references (leaves 203-228). Also available via World Wide Web.

Thesis (M.Ag.Sc. 1980) from the Department of Animal Physiology, University of Adelaide.

Thesis (M.Ag.Sci.)--University of Adelaide, Dept. of Animal Sciences, 1991. / Includes bibliographical references (leaves 59-79).

Thesis (M.Ag.Sc.)--University of Adelaide, Dept. of Animal Sciences, 1989. / Includes bibliographical references (leaves 196-220).