The cellular degradation of the low density lipoprotein (LDL) receptor, and its ligand, LDL, were investigated in order to clarify certain mechanistic aspects of these important processes. Long-term lymphoblastoid cell lines and cultured human skin fibroblasts were used to examine the fate of ¹²⁵I-LDL subsequent to its uptake via receptor-mediated endocytosis. In both cases, binding activity was saturable, depended on the presence of calcium ions in the medium, and was calculated to have an equilibrium dissociation constant at 4ᵒC of 2 μg ¹²⁵I-LDL/ml. No high-affinity binding was detected when the ligand was modified by acetylation. After incubating the monolayers at 37°C LDL/LDL receptor complexes were internalized, and the receptors were recycled back to the surface within about 10 minutes. Apolipo-protein B in the LDL particles was largely degraded to the amino acid level: chloroquine, a lysosomotropic agent, inhibited the formation of the ¹²⁵I-LDL degradation products. Cells obtained from a number of heterozygous and homozygous familial hypercholesterolemic patients, as expected, bound markedly reduced amounts of ligand. The half-life of ¹²⁵I-LDL was measured after it had been introduced into cultured fibroblasts by one of the following processes: (i) uptake via receptor-mediated endocytosis in human skin fibroblasts with normal LDL receptors, or (ii) incorporation via scrape-loading into fibroblasts defective in LDL receptor content. The half-lives obtained were about 1 hour and 50 hours, respectively, indicating that efficient degradation of LDL occurred only when it was deIivered to lysosomes via receptor-mediated endocytosis.

by Lee Hon Kit. / Thesis (M.Sc.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 80-89). / Chapter 1. --- Introduction --- p.1 / Chapter 1.1 --- Lipids and Lipoproteins --- p.1 / Chapter 1.1.1 --- Chemistry and Classification of Lipids --- p.1 / Chapter 1.1.2 --- Lipoprotein and Apolipoprotein --- p.3 / Chapter 1.1.2.1 --- Lipoprotein: Structure and Classification --- p.3 / Chapter 1.1.2.2 --- Apolipoprotein: Structure and Function --- p.5 / Chapter 1.1.2.3 --- Lipoprotein (a) and Apolipoprotein (a) --- p.8 / Chapter 1.1.3 --- Outline of Lipid and Lipoprotein Metabolism --- p.10 / Chapter 1.1.3.1 --- Exogenous Lipid Metabolism --- p.10 / Chapter 1.1.3.2 --- Endogenous Lipid Pathway --- p.13 / Chapter 1.2 --- "Dyslipidaemia: Definition, Classification and Coronary Heart Disease" --- p.20 / Chapter 1.2.1 --- Definition --- p.20 / Chapter 1.2.2 --- Classification of Dyslipidaemia --- p.21 / Chapter 1.2.3 --- Dyslipidaemia and CHD --- p.24 / Chapter 1.3 --- Dyslipoproteinaemia and Atherogenesis --- p.25 / Chapter 1.3.1 --- Pathology and Pathogenesis --- p.25 / Chapter 1.3.2 --- Central Role of Oxidised LDL in Atherogenesis --- p.29 / Chapter 1.3.3 --- LDL Heterogeneity and Atherogenesis --- p.37 / Chapter 1.4 --- Management of Dyslipidaemia --- p.41 / Chapter 1.4.1 --- Drug therapy --- p.43 / Chapter 1.4.1.1 --- Triglyceride Lowering Drugs --- p.43 / Chapter 1.4.1.2 --- Cholesterol Lowering Drugs --- p.45 / Chapter 1.4.1.3 --- Combination Drug Therapy --- p.46 / Chapter 1.5 --- Aims of this study --- p.49 / Chapter 2. --- Materials and Methods --- p.50 / Chapter 2.1 --- Materials --- p.50 / Chapter 2.1.1 --- Patients and Controls --- p.50 / Chapter 2.1.2 --- Drug Administration Trials --- p.51 / Chapter 2.1.3 --- Blood Samples --- p.52 / Chapter 2.1.4 --- Chemicals and Solutions --- p.52 / Chapter 2.1.5 --- Apparatus and Equipments --- p.52 / Chapter 2.2 --- Methods --- p.54 / Chapter 2.2.1 --- "Serum Cholesterol, Triglyceride and High Density Lipoprotein cholesterol" --- p.54 / Chapter 2.2.2 --- "Apolipoprotein AI, B-100 and Lipoprotein (a) Assays" --- p.54 / Chapter 2.2.3 --- Ultracentrifugation of LDL Fraction --- p.55 / Chapter 2.2.4 --- In Vitro Assessment of LDL Oxidisability --- p.55 / Chapter 2.2.4.1 --- De-Salting of LDL Fraction --- p.55 / Chapter 2.2.4.2 --- Continuously Diene Formation Monitoring --- p.56 / Chapter 2.2.5 --- LDL Particle Size --- p.56 / Chapter 2.2.6 --- Statistical Analysis --- p.57 / Chapter 3. --- Results --- p.59 / Chapter 3.1 --- Quantitative Measurement of apo B-100 --- p.59 / Chapter 3.2 --- "Associations between Serum Triglyceride, LDL Particle Size and LDL Oxidisability" --- p.60 / Chapter 3.3 --- "Effect of single drug and combination drug therapy on lipids, lipoproteins and apolipoproteins" --- p.64 / Chapter 3.3.1 --- Quantitative Changes of Lipids and Lipoproteins --- p.64 / Chapter 3.3.2 --- Qualitative changes of LDL particles --- p.65 / Chapter 4. --- Discussion --- p.74 / Chapter 4.1 --- "Associations between Triglyceride concentration, HDL Cholesterol concentration, LDL oxidisability and Particle Size" --- p.74 / Chapter 4.2 --- Effects of Fluvastatin and Gemfibrozil on Combined Hyperlipidaemic Patients --- p.76

Thesis (M.Sc.), Memorial University of Newfoundland, 2000. / Restricted until June 2003. Bibliography: leaves 98-117.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2006. / Härtill 4 uppsatser.

Thesis (M.Sc.)--Memorial University of Newfoundland, 1997. / Restricted until June 2000. Bibliography: leaves 230-274.

Thesis (M.Sc.)--Memorial University of Newfoundland, 2004. / Bibliography: leaves 93-115.

Thesis (Ph. D.)--Case Western Reserve University, 2006. / [School of Medicine] Department of Physiology and Biophysics. Includes bibliographical references. Available online via OhioLINK's ETD Center.

Wong Yuen Fan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 134-150). / Abstracts in English and Chinese. / ACKNOWLEDGMENTS --- p.i / ABSTRACT --- p.ii / LIST OF ABBREAIATIONS --- p.vii / TABLE OF CONTENTS --- p.ix / Chapter Chapter 1 --- General introduction / Chapter 1.1 --- History of Kudingcha --- p.1 / Chapter 1.2 --- Classification of Kudingcha --- p.1 / Chapter 1.3 --- Composition of Kudingcha --- p.3 / Chapter 1.4 --- Introduction to phenylethanoid glycosides --- p.4 / Chapter 1.4.1 --- Isolation and purification of phenylethanoid glycosides --- p.4 / Chapter 1.4.2 --- Taxonomy of phenylethanoid glycosides --- p.5 / Chapter 1.4.3 --- Structure of phenylethanoid glycosides --- p.5 / Chapter 1.4.4 --- Biosynthesis of phenylethanoid glycosides --- p.6 / Chapter 1.4.5 --- Pharmacological effects of phenylethanoid glycosides --- p.9 / Chapter 1.4.5.1 --- Anticarcinogenic activity --- p.10 / Chapter 1.4.5.2 --- Inhibitory activity of protein kinase C --- p.10 / Chapter 1.4.5.3 --- Immunosuppressive activity --- p.11 / Chapter 1.4.5.4 --- DNA repairing activity --- p.11 / Chapter 1.4.5.5 --- Antibacterial and antiviral activities --- p.11 / Chapter 1.4.5.6 --- Antiinflammatory and antinociceptive activities --- p.12 / Chapter 1.4.5.7 --- Hepatoprotective activity --- p.12 / Chapter 1.4.5.8 --- Inhibitory activity of xanthine oxidase --- p.13 / Chapter 1.4.5.9 --- Antioxidative and scavenging activities --- p.13 / Chapter Chapter 2 --- Isolation and purification of phenylethaonid glycosides in Kudingcha / Chapter 2.1 --- Introduction --- p.15 / Chapter 2.2 --- Objectives --- p.16 / Chapter 2.3 --- Materials and Methods --- p.17 / Chapter 2.3.1 --- Extraction and isolation --- p.17 / Chapter 2.3.2 --- High performance liquid chromatograph (HPLC)analysis --- p.19 / Chapter 2.3.2.1 --- "Acteoside, ligupurpuroside A and osmanthuside B" --- p.19 / Chapter 2.3.2.2 --- cis-Ligupurpuroside B and trans-ligupurpuroside B --- p.19 / Chapter 2.3.3 --- Isolation and purification of isoacteoside --- p.19 / Chapter 2.4 --- Results --- p.24 / Chapter 2.4.1 --- A cteoside --- p.24 / Chapter 2.4.2 --- Osmanthuside B --- p.24 / Chapter 2.4.3 --- Ligupurpuroside A --- p.24 / Chapter 2.4.4 --- trans-Ligupurpuroside B --- p.25 / Chapter 2.4.5 --- cis-Ligupurpuroside B --- p.25 / Chapter 2.4.6 --- Isoacteoside --- p.25 / Chapter 2.4.6.1 --- Thermal stability --- p.25 / Chapter 2.5 --- Discussions --- p.27 / Chapter 2.5.1 --- Acteoside --- p.27 / Chapter 2.5.2 --- Osmanthuside B --- p.27 / Chapter 2.5.3 --- Ligupurpuroside A --- p.28 / Chapter 2.5.4 --- trans-Ligupurpuroside B --- p.29 / Chapter 2.5.5 --- cis-Ligupurpuroside B --- p.29 / Chapter 2.5.6 --- Isoacteoside --- p.30 / Chapter Chapter 3 --- Inhibitory effect of phenylethanoid glycosides isolated from Kudingcha on Cu2+-mediated LDL oxidation in vitro / Chapter 3.1 --- Introduction --- p.36 / Chapter 3.2 --- Mechanisms of lipoprotein oxidation in vivo --- p.36 / Chapter 3.2.1 --- Oxidants underlying LDL oxidation --- p.36 / Chapter 3.2.2 --- Oxidative modification of LDL --- p.37 / Chapter 3.2.3 --- Role of oxidatively modified LDL in atherogenesis --- p.38 / Chapter 3.2.4 --- Antioxidants and atherosclerotic heart disease --- p.40 / Chapter 3.2.5 --- Measuring the thiobarbituric acid-reactive substances (TBARS) formation as an index to monitor LDL oxidation --- p.41 / Chapter 3.2.6 --- Effect of flavonoids on Cu2+-mediated human LDL oxidation --- p.41 / Chapter 3.3 --- Objectives --- p.43 / Chapter 3.4 --- Materials and methods --- p.44 / Chapter 3.4.1 --- LDL isolation --- p.44 / Chapter 3.4.2 --- LDL oxidation --- p.44 / Chapter 3.4.3 --- Thiobarbituric acid-reactive substances (TBARS) assay --- p.45 / Chapter 3.4.4 --- Interactions of phenylethanoid glycosides isolated from Kudingcha with Cu2+ in human LDL oxidation --- p.45 / Chapter 3.4.5 --- Statistics --- p.46 / Chapter 3.5 --- Results --- p.47 / Chapter 3.5.1 --- Protective effect of the major phenylethanoid glycosides isolated from Kudingcha on LDL oxidation --- p.47 / Chapter 3.5.2 --- Varying protective effect of individual major Kudingcha phenylethanoid glycosides --- p.47 / Chapter 3.5.3 --- Interactions of Kudingcha phenylethanoid glycosides with Cu2+in human LDL oxidation --- p.51 / Chapter 3.5 --- Discussions --- p.55 / Chapter Chapter 4 --- Inhibitory effects of Kudingcha phenylethanoid glycosides on a-tocopherol oxidation in vitro / Chapter 4.1 --- Introduction --- p.58 / Chapter 4.1.1 --- LDL oxidation and atherosclerosis --- p.58 / Chapter 4.1.2 --- Role of vitamin E in LDL lipid peroxidation --- p.59 / Chapter 4.1.3 --- Interaction of tocopherol interactions with other antioxidants and synergists --- p.61 / Chapter 4.2 --- Objectives --- p.62 / Chapter 4.3 --- Materials and Methods --- p.63 / Chapter 4.3.1 --- Depletion of a-tocopherol in LDL --- p.63 / Chapter 4.3.2 --- Regeneration of a-tocopherol in LDL --- p.63 / Chapter 4.3.3 --- HPLC analysis of a-tocopherol in LDL --- p.64 / Chapter 4.3.4 --- Statistics --- p.64 / Chapter 4.4 --- Results --- p.66 / Chapter 4.4.1 --- Protective effects of Kudingcha phenylethanoid glycosides on a-tocopherol depletion --- p.66 / Chapter 4.4.2 --- Regeneration of a-tocopherol by acteoside --- p.70 / Chapter 4.5 --- Discussions --- p.72 / Chapter Chapter 5 --- Relaxing effects of Kudingcha extract and purified acteoside in rat aortic rings / Chapter 5.1 --- Introduction --- p.75 / Chapter 5.1.1 --- Mechanisms of calcium mobilization --- p.76 / Chapter 5.1.1.1 --- Voltage-dependent calcium channel --- p.76 / Chapter 5.1.1.2 --- Thromboxane A2 Receptor-mediated calcium channel --- p.77 / Chapter 5.1.1.3 --- Protein kinase C in signal transudation --- p.77 / Chapter 5.1.2 --- Contractile proteins and regulation of contraction of vascular smooth muscle --- p.78 / Chapter 5.2 --- Objectives --- p.82 / Chapter 5.3 --- Materials and Methods --- p.83 / Chapter 5.3.1 --- Arterial ring preparation --- p.83 / Chapter 5.3.2 --- Vascular action of Kudingcha extract and acteoside --- p.85 / Chapter 5.3.2.1 --- Relaxant responses of Kudingcha extract and acteoside on U46619 -induced contraction --- p.85 / Chapter 5.3.2.2 --- Relaxant responses of Kudingcha extract and acteoside on high K+ and CaCl2-induced contraction --- p.85 / Chapter 5.3.2.3 --- Relaxant responses of Kudingcha extract and acteoside on protein kinase C- mediated contraction --- p.86 / Chapter 5.3.2.4 --- Effect of acteoside on acetylcholine-induced relaxation --- p.87 / Chapter 5.3.3 --- Statistics --- p.87 / Chapter 5.4 --- Results --- p.88 / Chapter 5.4.1 --- Effects of Kudingcha extract and acteoside on U46619-induced contraction --- p.88 / Chapter 5.4.2 --- Effects of Kudingcha extract and acteoside on high K+-induced contraction --- p.94 / Chapter 5.4.3 --- Effect of Kudingcha extract and acteoside on protein kinase C-mediated contraction --- p.98 / Chapter 5.4.4 --- Effect of acteoside on acetylcholine-induced relaxation --- p.100 / Chapter 5.5 --- Discussions --- p.103 / Chapter Chapter 6 --- Effect of Kudingcha on lipid contents of hamsters and New Zealand Rabbits / Chapter 6.1 --- Introduction --- p.106 / Chapter 6.1.1 --- Factors related to CHD --- p.106 / Chapter 6.1.2 --- Animal model --- p.107 / Chapter 6.2 --- Objectives --- p.108 / Chapter 6.3 --- Materials and Methods --- p.109 / Chapter 6.3.1 --- Rabbit --- p.109 / Chapter 6.3.1.1 --- Measurement of atheroma formation --- p.112 / Chapter 6.3.2 --- Hamster --- p.114 / Chapter 6.3.3 --- Serum lipid determinations --- p.116 / Chapter 6.3.4 --- Determination of hepatic cholesterol content --- p.116 / Chapter 6.3.5 --- Statistics --- p.117 / Chapter 6.4 --- Results --- p.119 / Chapter 6.4.1 --- Growth and Food intake --- p.119 / Chapter 6.4.2 --- "Effect of Kudingcha supplementation on Serum TG, TC and HDL-C" --- p.119 / Chapter 6.4.3 --- Effect of Kudingcha supplementation on hepatic cholesterol contents --- p.124 / Chapter 6.4.4 --- Effect of Kudingcha supplementation on atheroma formation --- p.124 / Chapter 6.5 --- Discussions --- p.129 / Chapter Chapter 7 --- Conclusions --- p.131 / References --- p.134

A hipercolesterolemia é o maior fator de risco para doença arterial coronária e é responsável por um número significante de doenças e mortes. Há evidências que o exercício físico diminui o risco cardiovascular exercendo efeitos benéficos sobre os fatores de risco, incluindo o metabolismo lipídico. Mudanças que ocorrem no metabolismo da LDL podem não ser detectadas através das dosagens rotineiras de lípides plasmáticos. Portanto, avaliamos os efeitos do exercício físico no metabolismo de uma nanoemulsão lipídica artificial com comportamento metabólico semelhante ao da LDL. Foram avaliados 12 indivíduos hipercolesterolêmicos sedentários (H) e 12 indivíduos normolipidêmicos sedentários (N) que foram submetidos a treinamento durante 4 meses. Nos grupos controle, foram estudados 8 indivíduos hipercolesterolêmicos sedentários controle (HC) e 8 indivíduos normolipidêmicos sedentários controle (NC) que não realizaram exercício físico. A emulsão marcada com éster de colesterol -14C (EC-14C) foi injetada endovenosamente. Amostras de sangue foram coletadas em tempos prédeterminados (5 min, 1, 2, 4, 6, 8, 24 horas) após a injeção, para determinação da radioatividade, das curvas de decaimento plasmático e cálculo da taxa fracional de remoção (TFR) dos lípides marcados, por análise compartimental. As avaliações foram feitas antes e após o protocolo de treinamento físico e nos grupos controle foram realizadas 2 avaliações, sendo a segunda 4 meses após a primeira. No grupo H, as concentrações plasmáticas de colesterol total e LDL-c diminuíram (5%, p= 0,0334 e 14%, p= 0,0058), respectivamente, enquanto que, HDL-c, TFR-EC-14C e lag time aumentaram (13%, p= 0,0142; 36%, p= 0,0187; 37%, p= 0,0039), respectivamente após o treinamento físico. No grupo N, a concentração plasmática da HDL foi maior (15%, p= 0,0243), após o treinamento. Nos grupos HC e NC os parâmetros avaliados foram semelhantes. Portanto, o exercício físico acelera a remoção plasmática da LDL em indivíduos hipercolesterolêmicos, indicado pela maior TFR-EC-14C. Este efeito pode ser um dos mecanismos pelos quais o exercício previne a doença arterial coronária. / Hypercholesterolemia has become one of the major risk factors for arterial coronary disease. As such, it is also responsible for a significant number of diseases and deaths. Evidence suggests that physical exercise can, in fact, decrease the risk of cardiovascular diseases by exerting beneficial effects upon the risk factors, including lipid metabolism. The changes that do occur in LDL metabolism are generally not detected by routine clinical laboratory plasma lipid exams. In the present study, the effects of physical exercise on the metabolism of an artificial lipidic nanoemoulsion with similar LDL metabolic behavior were analyzed. 12 hypercholesterolemic sedentary individuals (H) and 12 normolipidemic sedentary individuals (N) were studied. These 24 participants were submitted to a routine training program during a 4-month period. The control group was divided into two groups: one of 8 hypercholesterolemic sedentary individuals (CH) and the other with 8 normolipidemic sedentary individuals (CN) which did not partake in any exercise program. An emulsion labeled with 14Ccholesteryl ester (14C-CE) was endovenously injected into all 4 groups. Blood samples were collected at pre-determined periods (5 min, 1, 2, 4, 6, 8 and 24 hours) after the injection of the emulsion, in order to determine the radioactivity of the plasma decay curves and calculate the fractional clearance rate (FCR) of the labeled lipids for compartimental analysis. Evaluations were made before and after the exercise training protocol. The control groups under went 2 evaluations, the second one 4 months after the first evaluation. In the H group, total cholesterol and LDL-c plasma concentrations decreased (5%, p=0.0334 and 14%, p=0.0058), respectively. HDL-c, 14C-CE-FCR and lag time, on the other hand, increased (13%, p=0.0142; 36%, p=0.0187; 37%, p=0.0039) after exercise training. HDL plasma concentration for the N group was higher (15%, p=0.0243), after exercise training. In groups CH and CN the parameters evaluated were similar. Therefore, exercise accelerates the removal of LDL plasma in hypercholesterolemic individuals as indicated by a higher 14C-CE-FCR. This effect can thus be one of the mechanisms by which exercise can prevent arterial coronary disease.

Ho Hing Man. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (leaves 140-156). / Abstracts in English and Chinese. / Chapter Chapter 1 --- General introduction / Chapter 1.1 --- History of soybean --- p.1 / Chapter 1.2 --- Health benefits of soybean --- p.2 / Chapter 1.3 --- Introduction to flavonoids --- p.2 / Chapter 1.4 --- Bioavailability of flavonoids from foods --- p.3 / Chapter 1.5 --- Pharmacological effects of flavonoids and their glycosides --- p.4 / Chapter 1.5.1 --- Anticarcinogenic activity --- p.4 / Chapter 1.5.2 --- Antioxidative activity --- p.7 / Chapter 1.5.3 --- Cardioprotective activity --- p.9 / Chapter 1.5.4 --- Osteoprotective activity --- p.10 / Chapter 1.5.5 --- Neuroprotective activity --- p.12 / Chapter 1.5.6 --- Antiangiogenic activity --- p.12 / Chapter 1.6 --- Soy leaves --- p.13 / Chapter Chapter 2 --- Isolation and purification of kaempferol glycosides and genistin in soy leaves / Chapter 2.1 --- Introduction --- p.14 / Chapter 2.2 --- Objectives --- p.15 / Chapter 2.3 --- Materials and Methods --- p.16 / Chapter 2.3.1 --- Extraction and isolation --- p.16 / Chapter 2.3.1.1 --- Preparation of soy leaves butanol extract --- p.16 / Chapter 2.3.1.2 --- Preparation of kaempferol glycosides from soy leaves butanol extract --- p.16 / Chapter 2.3.2 --- High performance liquid chromatography (HPLC) analysis --- p.19 / Chapter 2.3.2.1 --- Sample preparation for the HPLC analysis --- p.19 / Chapter 2.3.2.2 --- HPLC analysis --- p.19 / Chapter 2.3.2.3 --- Quantification of the flavonoids and their glycosides --- p.23 / Chapter 2.3.2.4 --- Change in flavonoids and their glycosides in soy leaves --- p.23 / Chapter 2.4 --- Results --- p.24 / Chapter 2.4.1 --- Compound 1 --- p.24 / Chapter 2.4.2 --- Compound 2 --- p.24 / Chapter 2.4.3 --- Compound 3 --- p.25 / Chapter 2.4.4 --- Compound 4 --- p.25 / Chapter 2.4.5 --- Compound 5 --- p.25 / Chapter 2.4.6 --- Compound 6 --- p.26 / Chapter 2.4.7 --- Quantification of flavonoids in soybean and soy leaves --- p.32 / Chapter 2.4.8 --- Age-dependent changes in flavonoids and their glycosides --- p.32 / Chapter 2.5 --- Discussion --- p.35 / Chapter 2.5.1 --- Compound 1 --- p.35 / Chapter 2.5.2 --- Compound 2 --- p.35 / Chapter 2.5.3 --- Compound 3 --- p.37 / Chapter 2.5.4 --- Compound 4 --- p.38 / Chapter 2.5.5 --- Compound 5 --- p.39 / Chapter 2.5.6 --- Compound 6 --- p.40 / Chapter 2.5.7 --- Age-dependent changes in flavonoids and their glycosides --- p.40 / Chapter Chapter 3 --- Hypolipidemic effects of soy leaves in hamsters / Chapter 3.1 --- Introduction --- p.41 / Chapter 3.1.1 --- Different lipoproteins and their functions --- p.41 / Chapter 3.1.2 --- Risk factors of cardiovascular disease --- p.42 / Chapter 3.1.3 --- Animal model --- p.43 / Chapter 3.2 --- Objectives --- p.44 / Chapter 3.3 --- Materials and Methods --- p.45 / Chapter 3.3.1 --- Animals --- p.46 / Chapter 3.3.2 --- Serum lipid and lipoprotein determinations --- p.46 / Chapter 3.3.3 --- Determination of cholesterol in the liver and adipose tissue --- p.46 / Chapter 3.3.4 --- Extraction of neutral and acidic sterols from fecal samples --- p.49 / Chapter 3.3.4.1 --- Determination of neutral sterols --- p.49 / Chapter 3.3.4.2 --- Determination of acidic sterols --- p.50 / Chapter 3.3.4.3 --- GLC analysis of neutral and acidic sterols --- p.51 / Chapter 3.3.5 --- Statistics --- p.51 / Chapter 3.4 --- Results --- p.54 / Chapter 3.4.1 --- Growth and food intake --- p.54 / Chapter 3.4.2 --- "Effects of SLP and SLEE supplementation on serum triacylglycerol (TG), total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C)" --- p.54 / Chapter 3.4.3 --- Effects ofSLP and SLEE supplementation on non-HDL-C and ratio of non-HDL-C to HDL-C --- p.55 / Chapter 3.4.4 --- Effects of SLP amd SLEE supplementations on concentration of hepatic cholesterol --- p.58 / Chapter 3.4.5 --- Effects of SLP and SLEE supplementations on perirenal adipose tissue cholesterol --- p.58 / Chapter 3.4.6 --- Effects of SLP and SLEE supplementations on fecal neutral and acidic sterols --- p.61 / Chapter 3.5 --- Discussion --- p.64 / Chapter Chapter 4 --- Effects of soy leaves and its flavonoid glycosides on haemolysis and on LDL oxidation / Chapter 4.1 --- Introduction --- p.67 / Chapter 4.1.1 --- Role of low density lipoprotein oxidation in the development of atherosclerosis --- p.68 / Chapter 4.1.2 --- LDL oxidation --- p.70 / Chapter 4.1.3 --- Thiobarbituric acid reactive substances (TBARS) as an index of LDL oxidation --- p.71 / Chapter 4.1.4 --- Antioxidant and LDL oxidation --- p.74 / Chapter 4.2 --- Objective --- p.75 / Chapter 4.3 --- Materials and methods --- p.76 / Chapter 4.3.1 --- Isolation of LDL from human serum --- p.76 / Chapter 4.3.2 --- LDL oxidation --- p.77 / Chapter 4.3.3 --- Determine the formation of thiobarbituric acid-reactive substances (TBARS) --- p.77 / Chapter 4.3.4 --- Assay for erythrocyte haemolysis --- p.78 / Chapter 4.3.5 --- Statistics --- p.79 / Chapter 4.4 --- Results --- p.80 / Chapter 4.4.1 --- Effects of three different soy leaves extracts and flavonoid glycosides on LDL oxidation --- p.80 / Chapter 4.4.2 --- Effects of three soy leaves extracts and flavonoid glycosides on erythrocyte haemolysis --- p.80 / Chapter 4.5 --- Discussion --- p.85 / Chapter Chapter 5 --- Relaxing effects of soy leaves and its flavonoids / Chapter 5.1 --- Introduction --- p.89 / Chapter 5.1.1 --- Smooth muscle contraction --- p.90 / Chapter 5.1.1.1 --- Sliding filament mechanism --- p.91 / Chapter 5.1.2 --- Intracellular mechanisms involved in the regulation of smooth muscle contraction --- p.92 / Chapter 5.1.2.1 --- Voltage-gated Ca2+ channels --- p.92 / Chapter 5.1.2.2 --- Protein kinase C (PKC) mediated smooth muscle contraction --- p.93 / Chapter 5.1.2.3 --- Thromboxane A2 receptor-mediated calcium channel --- p.94 / Chapter 5.2 --- Objectives --- p.96 / Chapter 5.3 --- Materials and methods --- p.97 / Chapter 5.3.1 --- Drugs preparation --- p.97 / Chapter 5.3.2 --- Vessel preparation --- p.97 / Chapter 5.3.3 --- Contraction experiments --- p.99 / Chapter 5.3.3.1 --- Relaxant responses of soy leaves butanol extract on the contraction induced by different constrictors --- p.99 / Chapter 5.3.3.2 --- Relaxant responses of soy leaves butanol extract on U46619 and PGF2a- induced contraction --- p.99 / Chapter 5.3.3.3 --- "Relaxant responses of genistein, genistin and the kaempferol glycosides on U46619-induced contraction" --- p.100 / Chapter 5.3.4 --- Statistics --- p.100 / Chapter 5.4 --- Results --- p.102 / Chapter 5.4.1 --- Effect of soy leaves butanol extract --- p.102 / Chapter 5.4.2 --- Role of endothelium in extract-induced relaxation --- p.102 / Chapter 5.4.3 --- Effect of the soy leaves butanol extract on contractile response to prostaglandins --- p.103 / Chapter 5.4.4 --- Effects of kaempferol glycosides and kaempferol --- p.111 / Chapter 5.4.5 --- Effects of genistein and genistin --- p.111 / Chapter 5.5 --- Discussion --- p.118 / Chapter Chapter 6 --- Effect of soy leaves on mammary tumor / Chapter 6.1 --- Introduction --- p.123 / Chapter 6.1.1 --- Carcinogenesis --- p.123 / Chapter 6.1.1.1 --- In itiation --- p.124 / Chapter 6.1.1.2 --- Promotion --- p.124 / Chapter 6.1.1.3 --- Progression --- p.125 / Chapter 6.2 --- Objective --- p.126 / Chapter 6.3 --- Materials and methods --- p.127 / Chapter 6.3.1 --- Animal --- p.127 / Chapter 6.3.2 --- Determination of estrus cycle --- p.128 / Chapter 6.3.3 --- Statistics --- p.129 / Chapter 6.4 --- Results --- p.131 / Chapter 6.4.1 --- Incident rate of tumor induction --- p.131 / Chapter 6.4.2 --- Number of tumor induced --- p.131 / Chapter 6.5 --- Discussion --- p.136 / Chapter Chapter 7 --- Conclusions --- p.136 / References --- p.140