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It has been suggested that membrane characteristics associated with carcinomas could be related to an altered molecular structure of lipids inplasma membrane. The microsomal and soluble fractions of the cell are major sites of de novo synthesis and elongation/desaturation of fatty acids. It was the purpose of this study to compare the fatty acid composition of microsomal and soluble fractions isolated from mammary adenocarcinomas with that of normal mammary tissue and to determine if deviations found in the plasma membrane isolated from tumors could be observed at these subcellular levels.Microsomal and soluble fractions were isolated by differential centrifugation from mammary adenocarcinomas and from normal mammary tissue of Strain A female mice. Activities of nicotinamide adenine dinucleotide, reduced (NADH) dependent cytochrome c reductase andnicotinamide adenine dinucleotide phosphate, reduced (NADPH) dependent cytochrome c reductase in these fractions were determined. The fatty acids were extracted, methylated, and methyl esters identified and quantified using gas liquid chromatography. Polar and non-polar GLC columns, silver nitrate thin layer chromatography, hydrogenation, and spiking was used to confirm the identity of some fatty acids.Fatty acid composition of the microsomal and soluble fractions was similar in tumor and normal tissue. There was a greater percentage of C24:1 in tumors. A reversal of the oleic to stearic acid ratio, an increase in the level of palmitic acid, and a tendency toward long chain polyenoic fatty acids, as reported in studies on the plasma membrane isolated from tumors, was not evident in either the microsomal or soluble fractions. There was evidence of greater utilization of NADPH in the reduction of cytochrome c reductase in tumors. This may result in a decreased availability of NADPH for fatty acid synthetase and lipogenesis.Results of this study do not demonstrate support for a shift in the biosynthetic pathway for the synthesis of fatty acids in carcinomas. It is possible that changes in the lipid composition in the plasma membrane of tumor cells occur after initial incorporation or a shift in biosynthesis could occur in the mitochondria, another site of de novo synthesis and elongation/desaturation of fatty acids.

No description available.

Microplankton at five sites off South Georgia in January to February 1991 was dominated by a range of diatoms. The haptophyte Phaeocystis was present in three of the five sites but in low abundance only. Diatoms dominated at a more southerly site near the Antarctic Peninsula in March, whereas dinoflagellates dominated at a site near Deception Island. Multivariate analysis allowed the seven sites to be distinguished on the basis of microplankton species composition. Analysis of thirteen lipid classes present in total lipid extracted from the microplankton also demonstrated substantial differences from site to site. Multivariate analysis showed a different pattern of variation from the species ordination, with the South Georgia sites forming a distinct cluster. Outlier sites identified in the species and lipid ordinations confirmed the association between some taxonomic groups and lipid 'fingerprints'. Fatty acids extracted from total lipid in microplankton at five sites around South Georgia and two sites near the Antarctic Peninsula ranged from 37 to 195 J.Lg1-1, with a ratio of fatty acids in polar lipid: neutral lipid ranging from 4: 1 to 1:2. A further eleven particulate samples analysed from sites around the Antarctic Peninsula had slightly lower fatty acid content with a mean of 50 J.Lg1-1. Fatty acids in polar lipid were rich in (n-3) polyunsaturated fatty acids, chiefly 20:5(n-3). However, 22:6(n-3) could be as abundant as 20:5(n-3) in polar lipid from microplankton less than 20 J.1m, and also in dinoflagellate-rich microplankton. Neutral lipid was dominated by 16:0, 16:1(n-7) and 18:1(n-9) fatty acids and contained only low levels of (n-3) polyunsaturated fatty acids. The data reveal the high nutritional quality of microplankton lipids in the Southern Ocean for filter feeding animals, including krill. Samples of krill from eight sites around South Georgia consisted predominantly of immature animals, and females were entirely absent from samples from two of the eight sites studied. Animal wet mass varied from 0.16-1.72 g (median values of 0.47, 1.15 and 1.46 g for immatures, males and females respectively). Lipid amounts varied from 5-147 mg per animal (median values of 17.8, 21.0 and 73.3 mg for immatures, males and females respectively). Triacylglycerol (TAG) and phosphatidylcholine were the two most abundant lipid classes in all animals. Multivariate analysis of lipid composition indicated significant overlap between sex-maturity classes, although female krill tended to be distinguished from males by higher proportions of TAG and lower proportions of phosphatidylserine plus phosphatidylinositol. Reproductive investment is implicated in the overall variability in lipid content and composition, with females containing high lipid levels as reserves for egg production, whilst males showed apparent lipid deficits resulting from short-term mobilisation of storage material for spermatophore production and attachment. Significant and systematic site-to-site variability in lipid content and composition were evident in the samples and this could not be explained by the sex ratio or animal size. Such variability might have arisen from local patterns of krill distribution but could not be ascribed simply to temporal changes in lipid during the study. Immature Antarctic krill (length 40-45 mm) maintained in an aquarium for up to nine months were fed dense suspensions of cultures of two algal taxa, the haptophyte /sochrysis and the diatom Thalassiosira. Following acclimation to the experimental feeding regime, the animals were transferred to identical containers holding cultures of the same alga already labelled with [14C]bicarbonate. Faecal pellets collected after transfer showed detectable radioactivity after 30 minutes for /sochrysis and 55 minutes for Thalassiosira, providing an estimation of gut throughput time. With both algal cultures, radioactivity in faecal pellets increased over the 4-5 hour collection period. However, whilst faecal pellets derived from Isochrysis showed a rapid initial increase followed by an approach to a plateau value, the radioactivity in Thalassiosira-derived pellets increased steadily. A first-order kinetic model fitted to these data showed a more rapid turnover time for Isochrysis (k = 47 min) than for Thaiassiosira (k = 256 min). The assimilation efficiency based on the ratio of ingested radiolabelled lipid to that egested in faeces was 86% for /sochrysis and 63% for Thalassiosira, whereas corresponding efficiencies calculated from mass lipid budgets were 75% for /sochrysis and 77% for Thalassiosira. Analysis of fatty acid content and composition of total lipid from algae, krill and faecal pellets established that all dietary fatty acids were very efficiently ssimilated although there was a relatively preferential excretion of saturated fatty acids. All the assimilated fatty acids were extensively catabolised with the possible exceptions of saturated fatty acids and 18:4. Evidence was obtained for some biosynthesis of saturated fatty acids from non-lipid dietary precursors and for a limited conversion of 18:3 to 18:4 Collating the data presented in this thesis in a budget indicates that under suitable conditions, Euphausia superba is capable of acquiring the lipid necessary for growth and reproduction over time scales of only a few weeks and certainly within a single summer. Hence, krill appears to be an animal capable of high energy throughput and high reproductive output.

Migraine is associated with a number of cardiometabolic risk factors including abnormalities in lipid metabolism. However, little is known about these associations among pregnant migraineurs. We conducted the present study to evaluate the extent to which altered lipid profiles are associated with history of migraine among pregnant women.

The aim of this thesis was to assess the effect of different of intake of polyunsaturated fatty acids on indices of oxidative stress, particularly damage to lipids and DNA and to examine whether this effect could be modified by supplementation with the lipid soluble antioxidant, vitamin E. This was assessed using a split plot/change over dietary study, where half and volunteers consumed a diet containing 5% PUFA (low PUFA) as food energy for 4 weeks and after a washout period of up to 10 weeks, consumed a 15% PUFA (high PUFA) diet for another 4 weeks. The other volunteers completed this protocol in reverse. Total fat, carbohydrates and protein, and vitamins E and C contents of the diets were constant and they were provided either with or without an additional 80mg d-tocopherol acetate/day. The results showed that although plasma total cholesterol showed a small significant increase after the low PUFA diets there was no change after consumption of the high PUFA diets or either of the vitamin E supplemented diets. Indices of oxidative stress (whole blood oxidised glutathione and urinary thiobarbituric acid reactive substances (TBARS)) were increased following consumption of the high PUFA diet. However, there was no change in non-specific plasma indices of lipid peroxidation, conjugated dienes and TBARS, nor in red cell antioxidant enzymes, glutathione reductase, and catalase. These results indicate that increasing dietary levels of PUFA may adversely affect some indices of lipid peroxidation, DNA damage and antioxidant status whilst not appearing to improve lipoprotein profiles. Increasing the dietary intake of vitamin E appears to ameliorate the potentially damaging effects of PUFA. Therefore, care should be taken when providing dietary advice on PUFA intake and an adequate intake of antioxidants to match any increased PUFA may be important for preventing oxidative stress.

Thesis (M.Sc.(Med.)--University of the Witwatersrand, Faculty of Health Sciences, 2000.

by Siu-fan Fung. / Thesis (M.Sc.)--Chinese University of Hong Kong, 1992. / Includes bibliographical references (leaves 89-104). / Title --- p.1 / Acknowledgement --- p.2 / Contents --- p.3 / Abstract --- p.6 / List of Tables --- p.9 / List of Figures --- p.12 / Reference Ranges --- p.14 / Abbreviations --- p.15 / Chapter 1. --- Introduction --- p.16 / Chapter 1.1. --- "Clinical biochemistry of lipids, apolipoproteins and lipoproteins" --- p.16 / Chapter 1.1.1. --- Lipids: definition and physiological importance --- p.16 / Chapter 1.1.2. --- Lipoproteins and apolipoproteins --- p.16 / Chapter 1.1.3. --- Lipoprotein metabolism --- p.19 / Chapter 1.1.3.1. --- Digestion and absorption of lipids --- p.19 / Chapter 1.1.3.2. --- Exogenous lipoprotein metabolism --- p.20 / Chapter 1.1.3.3. --- Endogenous lipoprotein metabolism --- p.21 / Chapter 1.1.4. --- Dyslipoproteinaemia and atherosclerosis --- p.22 / Chapter 1.1.4.1. --- Risk factos associated with atherosclerosis --- p.22 / Chapter 1.1.4.2. --- "Plasma cholesterol, lipoproteins and atherosclerosis" --- p.23 / Chapter 1.1.4.3. --- Plasma triglyceride and atherosclerosis --- p.25 / Chapter 1.1.4.4. --- "Apolipoprotein A-I (apo A-I), apolipoprotein B (apo B) and atherosclerosis" --- p.25 / Chapter 1.1.4.5. --- Postprandial lipidaemia and atherosclerosis --- p.26 / Chapter 1.2. --- Lipid metabolism in diabetes mellitus --- p.29 / Chapter 1.2.1. --- Diabetes mellitus --- p.29 / Chapter 1.2.2. --- Lipoprotein metabolism in non-insulin dependent diabetes mellitus ( NIDDM ) --- p.30 / Chapter 1.3. --- Lipid tolerance test --- p.32 / Chapter 1.3.1. --- General discussion --- p.32 / Chapter 1.3.2. --- Use of Maxolon --- p.33 / Chapter 1.4. --- Objectives --- p.34 / Chapter 2. --- Materials and methods --- p.36 / Chapter 2.1 --- Materials --- p.36 / Chapter 2.2 --- Subjects and patients --- p.37 / Chapter 2.2.1. --- Healthy subjects --- p.37 / Chapter 2.2.2. --- NIDDM patients --- p.37 / Chapter 2.2.3. --- Glucose intolerant (IGT) patients --- p.37 / Chapter 2.2.4 --- Study design --- p.38 / Chapter 2.3. --- Blood samples --- p.39 / Chapter 2.3.1. --- Serum samples --- p.39 / Chapter 2.3.2. --- Serum triglyceride-rich lipoproteins (TRL) fraction --- p.39 / Chapter 2.4. --- Analytical methods --- p.40 / Chapter 2.4.1. --- Cholesterol --- p.40 / Chapter 2.4.2. --- Triglyceride --- p.40 / Chapter 2.4.3. --- HDL-cholesterol --- p.41 / Chapter 2.4.4. --- Apo A-1 and Apo-B --- p.41 / Chapter 2.5. --- Measurement of postprandial serum triglyceride and TRL triglyceride --- p.42 / Chapter 2.6. --- Statistical analysis --- p.42 / Chapter 3. --- Results --- p.44 / Chapter 4. --- Discussion --- p.78 / References --- p.89