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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Mushroom-derived preparations in the prevention of oxidative damage to cellular DNA. / CUHK electronic theses & dissertations collection / Digital dissertation consortium

January 2001 (has links)
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.
2

Antimicrobial properties of monolaurin and selected antioxidants in vitro and in ground pork

Cheng, Tai Ben. January 1985 (has links)
Call number: LD2668 .T4 1985 C475 / Master of Science
3

Antioxidant and antiproliferative activities of flower tea extracts.

January 2007 (has links)
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
4

The antioxidative and hypolipidemic activities of hawthorn fruit. / CUHK electronic theses & dissertations collection

January 2001 (has links)
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.
5

Efeito da suplementação de β-caroteno sintético no DNA e no metabolismo de células hepáticas de ratos recebendo etanol / Effect of synthetic (β-carotene supplementattion in the DNA and metabolism of hepatic cells of rats receiving ethanol

Zanuto, Marcia Elena 03 May 2005 (has links)
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.
6

Efeito da suplementação de &#946;-caroteno sintético no DNA e no metabolismo de células hepáticas de ratos recebendo etanol / Effect of synthetic (&#946;-carotene supplementattion in the DNA and metabolism of hepatic cells of rats receiving ethanol

Marcia Elena Zanuto 03 May 2005 (has links)
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.

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