by Shi Yuling. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (p. 159-184). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Call number: LD2668 .T4 1985 C475 / Master of Science

Leung, Yu Tim. / Thesis submitted in: November 2006. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 103-128). / Abstracts in English and Chinese. / Thesis Committee --- p.i / Acknowledgements --- p.ii / Abstract --- p.iii / 摘要 --- p.iv / Table of Contents --- p.v / List of Tables --- p.ix / List of Figures --- p.x / Abbreviations --- p.xiii / Chapter 1. --- Introduction / Chapter 1.1 --- Flower herbal teas --- p.1 / Chapter 1.2 --- R. rugosa --- p.3 / Chapter 1.2.1 --- The phytochemistry of R. rugosa --- p.3 / Chapter 1.3 --- Secondary metabolites --- p.4 / Chapter 1.4 --- Classification of secondary metabolites --- p.6 / Chapter 1.5 --- Phenolic compounds --- p.6 / Chapter 1.5.1 --- Phenylpropanoid compounds --- p.6 / Chapter 1.5.2 --- Lignins --- p.7 / Chapter 1.5.3 --- Coumarins --- p.7 / Chapter 1.5.4 --- Stilbenes --- p.8 / Chapter 1.5.5 --- Tannins --- p.8 / Chapter 1.5.6 --- Flavonoids --- p.9 / Chapter 1.6 --- Oxidative Stress --- p.13 / Chapter 1.6.1 --- Diseases related to ROS --- p.13 / Chapter 1.6.2 --- Significant chemical or biochemical conversion of ROS --- p.14 / Chapter 1.6.3 --- Sources of ROS --- p.15 / Chapter 1.7 --- Natural dietary antioxidants --- p.15 / Chapter 1.7.1 --- Vitamin C --- p.15 / Chapter 1.7.2 --- Vitamin E --- p.16 / Chapter 1.7.3 --- Carotenoids --- p.16 / Chapter 1.7.4 --- Phenolic compounds --- p.16 / Chapter 1.8 --- Cancinogenesis --- p.17 / Chapter 1.9 --- Cell cycle --- p.18 / Chapter 1.9.1 --- Cell cycle of eukaryotic cells --- p.18 / Chapter 1.9.2 --- Checkpoints of cell cycle --- p.18 / Chapter 1.10 --- Cancer cell lines --- p.19 / Chapter 1.11 --- The growth phases of cancer cell lines --- p.20 / Chapter 1.12 --- Antiproliferative effects of phenolic compounds --- p.21 / Chapter 1.13 --- Genotoxicity of phenolic compounds --- p.22 / Chapter 1.14 --- Objectives --- p.23 / Chapter 2. --- Methods and Materials / Chapter 2.1 --- Extraction of active substances --- p.40 / Chapter 2.2 --- Determination of antioxidant activities TEAC assay --- p.40 / Chapter 2.3 --- Determination of hydroxy 1 radical scavenging activity by the deoxyribose assay --- p.41 / Chapter 2.4 --- Determination of phenolic contents by Folin´ؤCiocalteu assay --- p.43 / Chapter 2.5 --- Determination of total flavonoid by aluminum chloride colorimetric method --- p.43 / Chapter 2.6 --- Determination of oxidative DNA damage by comet assay --- p.44 / Chapter 2.7 --- Cell lines propagation --- p.49 / Chapter 2.8 --- Determination of antiproliferative activities by MTT assay (colorimetric) --- p.50 / Chapter 2.9 --- Determination of antiproliferative activities by BrdU labeling assay --- p.52 / Chapter 2.10 --- Cell cycle analysis by flow cytometry --- p.55 / Chapter 2.11 --- Determination of genotoxicity by SOS chromotest --- p.57 / Chapter 3. --- Results / Chapter 3.1 --- Dermination of antioxidant activities by TEAC assay --- p.59 / Chapter 3.1.1 --- Trolox Standard Reference --- p.59 / Chapter 3.1.2 --- TEAC of the seven flower extracts --- p.59 / Chapter 3.2 --- Hydroxyl radical scavenging activity by deoxyribose assay --- p.60 / Chapter 3.3 --- Determination of phenolic contents by Folin´ؤCiocalteu assay --- p.60 / Chapter 3.4 --- Determination of total flavonoids by colorimetirc aluminium chloride assay --- p.61 / Chapter 3.5 --- "The Inter-correlation between the antioxidant activities, total phenolic and flavonoid contents of flower extraction powders" --- p.61 / Chapter 3.6 --- Determination of oxidative DNA damage by comet assay --- p.62 / Chapter 3.7 --- Determination of antiproliferative activities by MTT assay --- p.63 / Chapter 3.7.1 --- Antiporoliferative activities on HepG2 --- p.63 / Chapter 3.7.2 --- Antiproliferative activities on MCF7 --- p.63 / Chapter 3.7.3 --- IC50 of R. rugosa extract on both HepG2 and MCF7 --- p.64 / Chapter 3.8 --- "The Inter-correlation between antioxidant activities, total phenolic contents, flavonoid contents, and the antiproliferative activities of flower extraction Powders" --- p.64 / Chapter 3.9 --- Determination of DNA synthesis by BrdU labeling analysis --- p.65 / Chapter 3.10 --- Cell cycle analysis by flow cytometry --- p.65 / Chapter 3.11 --- Determination of genotoxicity by SOS chromotest --- p.66 / Chapter 4. --- Discussions / Chapter 4.1 --- Extraction method --- p.90 / Chapter 4.2 --- Comparison of TEAC of the dry flowers with other foods --- p.90 / Chapter 4.3 --- Correlation between ABTS+ and hydroxyl scavenging ability of flower extraction powder --- p.91 / Chapter 4.4 --- Comparison of phenolic contents of the fry flowers with other foods --- p.92 / Chapter 4.5 --- Correlation between total phenolic contents and flavonoid contents of flower Eextraction powders --- p.92 / Chapter 4.6 --- "Correlation between total phenolic, flavonoid content and antioxidant activities of flower extraction powders" --- p.93 / Chapter 4.7 --- Factors affecting the antioxidant power besides total phenolic contents --- p.94 / Chapter 4.8 --- Synergistic effect of phenolic compounds --- p.94 / Chapter 4.9 --- Toxicity of drinking flower herbal tea --- p.95 / Chapter 4.10 --- Recommended dose of flower herbal teas --- p.96 / Chapter 4.11 --- Antiproliferative activities of flower extracts by MTT assay --- p.97 / Chapter 4.12 --- Antiproliferation activities of flower extraction Powders by Brdu labeling assay --- p.98 / Chapter 4.13 --- Protective effects of flower extraction powder on oxidative DNA damage determined by comet assay --- p.99 / Chapter 4.14 --- Cell cycle analysis --- p.100 / Chapter 4.15 --- Further Studies --- p.101 / Chapter 5. --- Conclusion --- p.102 / Chapter 6. --- References --- p.103

by Zhang Ze Sheng. / "October 2001." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (p. 157-174). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

A suplementação de &#946;-caroteno em fumantes e alcoólatras pode promover efeitos indesejáveis, manifestando a característica pró-oxidante deste carotenóide. Sabendo que o fígado é o principal órgão de armazenamento de vitamina A e (&#946;-caroteno, e local de oxidação do etanol, o presente estudo buscou investigar no fígado de ratos, a influência da suplementação de (&#946;-caroteno isolado ou associado ao etanol, sobre o metabolismo celular, danos no DNA, proliferação celular e função da proteína p53. Os ratos receberam dietas líquidas contendo (&#946;-caroteno (24mg/L dieta) com (GAB) ou sem (GBC) a adição de etanol (36% da calorias totais da dieta) e dieta líquida normal (isenta de &#946;-caroteno e etanol) (GDN), durante seis semanas de período experimental. Após este período, os animais foram sacrificados para determinações hepáticas e plasmáticas de (&#946;-caroteno, retinol, palmitato de retinila, presença de esteatose, determinações hepáticas de SRATB e GSH, danos no DNA de hepatócitos e expressão do PCNA e da proteína p53. Os resultados mostraram diferenças (p<0,05) entre os grupos quanto as concentrações hepáticas de retinol (&#181;g/g) (GAB: 2,49 ± 0,25; GBC: 4,22 ± 0,24; GDN: 2,83 ± 0,21) e palmitato de retinila (&#181;g/g) (GAB: 40,87 ± 3,98; GBC: 83,72 ± 6,00; GDN: 46,33 ± 3,60), concentração plasmática de retinol (llmol/L) (GAB: 1,42 ± 0,12; GBC: 0,69 ± 0,06; GDN: 2,37 ± 0,28), presença de esteatose (GAB: 2,30 ± 0,21; GBC: 1,00 ± 0,00; GDN: 1,00 ± 0,00), danos no DNA de hepatócitos (danos DNA/100 hepatócitos) (GAB: 285,90 ± 15,20; GBC: 273,83 ± 13,39; GDN: 138,00 ± 4,04) e expressão do PCNA (%0) (GAB: 7,12 ± 1,46; GBC: 1,47 ± 0,27; GDN: 2,04 ± 0,31). As concentrações hepáticas e plasmáticas de &#946;-caroteno, SRATB e GSH hepáticos, não apresentaram diferença (p>0,05) entre os grupos. A proteína p53 não foi expressa em nenhum dos grupos estudados. Estes resultados mostraram que o (&#946;-caroteno isolado e em associação com o etanol não influenciaram na peroxidação lipídica e na expressão da proteína p53. A associação &#946;-caroteno + etanol foi mais prejudicial ao fígado, promovendo alterações no metabolismo celular dos hepatócitos, esteatose, danos no DNA e proliferação celular, considerando que o &#946;-caroteno isolado foi genotóxico ao hepatócito. / &#946;-carotene, when supplemented in smokers and alcohol drinkers may act as prooxidant, resulting in undesirable effects. The liver is the &#946;-carotene and vitamin A main storage organ and where ethanol oxidation takes place. This study investigated in rats\' liver, the influence of &#946;-carotene supplementation either alone or associated with ethanol in cellular metabolism, DNA damage, cellular proliferation and p53 protein function. Three groups of 12 rats received liquid diets containing &#946;-carotene (24mg/L diet) with (BAG) or without (CBG) ethanol (36% of total energy intake). Control animals received liquid diet free of ethanol and &#946;-carotene (NDG). After 6 weeks the animals were sacrificed for hepatic and plasma concentrations of &#946;-carotene, retinol, palmitate retinyl, steatosis, GSH and TBARS, DNA damage, PCNA and p53 expression were evaluated in the liver. Differences were significant for hepatic (BAG: 2.49 ± 0.25; CBG: 4.22 ± 0.24; NDG: 2.83 ± 0.21 mg/g) and plasmatic (BAG: 1.42 ± 0.12; CBG: 0.69 ± 0.06; NDG: 2,37 ± 0,28mmol/L) retinol and hepatic palmitate retinyl (BAG: 40.87 ± 3.98; CBG: 83.72 ± 6.00; NDG: 46.33 ± 3.60), steatosis (BAG: 2.30 ± 0.21; CBG: 1.00 ± 0.00; NDG: 1.00 ± 0.00), DNA damage (BAG: 285.90 ± 15.20; CBG: 273.83 ± 13.39; NDG: 138.00 ±4.04 DNA damages/100 hepatocytes) and PCNA expression (BAG: 7.12 ± 1.46; CBG: 1.47 ± 0.27; NDG: 2.04 ± 0.31) among the groups (p<0.05). Hepatic and plasmatic concentrations of &#946;carotene, TBARS and GSH were not statistically different. p53 staining was not detected in any group. This suggests that &#946;-carotene alone or with ethanol association does not influence lipid peroxidation and p53 expression. &#946;-carotene+ethanol caused metabolic alteration, steatosis, DNA damage and cellular proliferation in hepatocytes. Furthermore, supplementation with &#946;-carotene alone had genotoxic effects in the liver.

A suplementação de &#946;-caroteno em fumantes e alcoólatras pode promover efeitos indesejáveis, manifestando a característica pró-oxidante deste carotenóide. Sabendo que o fígado é o principal órgão de armazenamento de vitamina A e (&#946;-caroteno, e local de oxidação do etanol, o presente estudo buscou investigar no fígado de ratos, a influência da suplementação de (&#946;-caroteno isolado ou associado ao etanol, sobre o metabolismo celular, danos no DNA, proliferação celular e função da proteína p53. Os ratos receberam dietas líquidas contendo (&#946;-caroteno (24mg/L dieta) com (GAB) ou sem (GBC) a adição de etanol (36% da calorias totais da dieta) e dieta líquida normal (isenta de &#946;-caroteno e etanol) (GDN), durante seis semanas de período experimental. Após este período, os animais foram sacrificados para determinações hepáticas e plasmáticas de (&#946;-caroteno, retinol, palmitato de retinila, presença de esteatose, determinações hepáticas de SRATB e GSH, danos no DNA de hepatócitos e expressão do PCNA e da proteína p53. Os resultados mostraram diferenças (p<0,05) entre os grupos quanto as concentrações hepáticas de retinol (&#181;g/g) (GAB: 2,49 ± 0,25; GBC: 4,22 ± 0,24; GDN: 2,83 ± 0,21) e palmitato de retinila (&#181;g/g) (GAB: 40,87 ± 3,98; GBC: 83,72 ± 6,00; GDN: 46,33 ± 3,60), concentração plasmática de retinol (llmol/L) (GAB: 1,42 ± 0,12; GBC: 0,69 ± 0,06; GDN: 2,37 ± 0,28), presença de esteatose (GAB: 2,30 ± 0,21; GBC: 1,00 ± 0,00; GDN: 1,00 ± 0,00), danos no DNA de hepatócitos (danos DNA/100 hepatócitos) (GAB: 285,90 ± 15,20; GBC: 273,83 ± 13,39; GDN: 138,00 ± 4,04) e expressão do PCNA (%0) (GAB: 7,12 ± 1,46; GBC: 1,47 ± 0,27; GDN: 2,04 ± 0,31). As concentrações hepáticas e plasmáticas de &#946;-caroteno, SRATB e GSH hepáticos, não apresentaram diferença (p>0,05) entre os grupos. A proteína p53 não foi expressa em nenhum dos grupos estudados. Estes resultados mostraram que o (&#946;-caroteno isolado e em associação com o etanol não influenciaram na peroxidação lipídica e na expressão da proteína p53. A associação &#946;-caroteno + etanol foi mais prejudicial ao fígado, promovendo alterações no metabolismo celular dos hepatócitos, esteatose, danos no DNA e proliferação celular, considerando que o &#946;-caroteno isolado foi genotóxico ao hepatócito. / &#946;-carotene, when supplemented in smokers and alcohol drinkers may act as prooxidant, resulting in undesirable effects. The liver is the &#946;-carotene and vitamin A main storage organ and where ethanol oxidation takes place. This study investigated in rats\' liver, the influence of &#946;-carotene supplementation either alone or associated with ethanol in cellular metabolism, DNA damage, cellular proliferation and p53 protein function. Three groups of 12 rats received liquid diets containing &#946;-carotene (24mg/L diet) with (BAG) or without (CBG) ethanol (36% of total energy intake). Control animals received liquid diet free of ethanol and &#946;-carotene (NDG). After 6 weeks the animals were sacrificed for hepatic and plasma concentrations of &#946;-carotene, retinol, palmitate retinyl, steatosis, GSH and TBARS, DNA damage, PCNA and p53 expression were evaluated in the liver. Differences were significant for hepatic (BAG: 2.49 ± 0.25; CBG: 4.22 ± 0.24; NDG: 2.83 ± 0.21 mg/g) and plasmatic (BAG: 1.42 ± 0.12; CBG: 0.69 ± 0.06; NDG: 2,37 ± 0,28mmol/L) retinol and hepatic palmitate retinyl (BAG: 40.87 ± 3.98; CBG: 83.72 ± 6.00; NDG: 46.33 ± 3.60), steatosis (BAG: 2.30 ± 0.21; CBG: 1.00 ± 0.00; NDG: 1.00 ± 0.00), DNA damage (BAG: 285.90 ± 15.20; CBG: 273.83 ± 13.39; NDG: 138.00 ±4.04 DNA damages/100 hepatocytes) and PCNA expression (BAG: 7.12 ± 1.46; CBG: 1.47 ± 0.27; NDG: 2.04 ± 0.31) among the groups (p<0.05). Hepatic and plasmatic concentrations of &#946;carotene, TBARS and GSH were not statistically different. p53 staining was not detected in any group. This suggests that &#946;-carotene alone or with ethanol association does not influence lipid peroxidation and p53 expression. &#946;-carotene+ethanol caused metabolic alteration, steatosis, DNA damage and cellular proliferation in hepatocytes. Furthermore, supplementation with &#946;-carotene alone had genotoxic effects in the liver.