Li, Yanhong. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 192-212). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Keung Hoi Yee. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (leaves 151-174). / Abstracts in English and Chinese. / Acknowledgement --- p.I / Abstract --- p.II / 摘要 --- p.V / Content --- p.VII / List of tables --- p.XIII / List of figures --- p.XIV / Abbreviations --- p.XVII / Chapter Chapter 1 --- General Introduction --- p.1 / Chapter 1.1 --- Biology of Pleurotus tuber-regiun (Ptr) --- p.1 / Chapter 1.1.1 --- Ptr grown in the wild --- p.1 / Chapter 1.1.2 --- Cultivation of Ptr --- p.2 / Chapter 1.2 --- Functional food and pharmaceutical application of Ptr sclerotium --- p.3 / Chapter 1.2.1 --- Traditional food and medicinal uses of Ptr sclerotium --- p.3 / Chapter 1.2.2 --- Nutritional value and chemical composition --- p.4 / Chapter 1.2.3 --- Anti-tumor activity --- p.7 / Chapter 1.2.4 --- Anti-viral activity --- p.8 / Chapter 1.2.5 --- Immunologic function --- p.8 / Chapter 1.2.6 --- Pharmaceutical application --- p.9 / Chapter Chapter 2 --- Toxicological evaluation on Ptr sclerotium --- p.11 / Chapter 2.1 --- Introduction --- p.11 / Chapter 2.1.1 --- Toxicological concern of Ptr sclerotium --- p.11 / Chapter 2.1.2 --- Toxicological study --- p.12 / Chapter 2.1.3 --- Biochemical methods for toxicological evaluation --- p.14 / Chapter 2.1.3.1 --- Serum enzyme activities --- p.15 / Chapter 2.1.3.2 --- Other serum analytes --- p.17 / Chapter 2.1.4 --- Histopathological study --- p.20 / Chapter 2.1.5 --- Acute toxicity --- p.21 / Chapter 2.1.6 --- Sub-acute and sub-chronic toxicity --- p.23 / Chapter 2.1.7 --- Objectives --- p.26 / Chapter 2.2 --- Materials and Methods --- p.27 / Chapter 2.2.1 --- Sample materials and chemicals --- p.27 / Chapter 2.2.2 --- Acute toxicity test --- p.27 / Chapter 2.2.2.1 --- Diet and animals --- p.27 / Chapter 2.2.2.2 --- Experimental design --- p.28 / Chapter 2.2.2.3 --- Calculation of sclerotium intake dose --- p.29 / Chapter 2.2.2.4 --- Biochemical assays --- p.30 / Chapter 2.2.2.5 --- Histopathological examination --- p.31 / Chapter 2.2.3 --- Sub-acute and sub-chronic toxicity tests --- p.32 / Chapter 2.2.3.1 --- Diet Preparation --- p.32 / Chapter 2.2.3.2 --- Experimental design --- p.32 / Chapter 2.2.3.3 --- Biochemical assays --- p.36 / Chapter 2.2.3.4 --- Organ weight --- p.40 / Chapter 2.2.3.5 --- Histopathological examination --- p.41 / Chapter 2.2.4 --- Statistical analyses --- p.41 / Chapter 2.3 --- Results and Discussion --- p.42 / Chapter 2.3.1 --- Acute toxicity test --- p.42 / Chapter 2.3.1.1 --- Food consumption --- p.43 / Chapter 2.3.1.2 --- Serum transaminase activities --- p.44 / Chapter 2.3.1.3 --- Histopathology --- p.45 / Chapter 2.3.1.4 --- NOAEL --- p.45 / Chapter 2.3.2 --- Sub-acute toxicity test --- p.50 / Chapter 2.3.2.1 --- Body weight gain --- p.50 / Chapter 2.3.2.2 --- Biochemical assays --- p.51 / Chapter 2.3.2.3 --- Organ per body weight and histopathology --- p.52 / Chapter 2.3.2.4 --- Effects of Ptr sclerotial diets --- p.53 / Chapter 2.3.3 --- Sub-chronic toxicity test --- p.59 / Chapter 2.3.3.1 --- Food and energy consumption --- p.59 / Chapter 2.3.3.2 --- Biochemical assays --- p.63 / Chapter 2.3.3.3 --- Organ per body weight --- p.67 / Chapter 2.3.3.4 --- Body weight increase --- p.75 / Chapter 2.3.3.5 --- NOAEL --- p.80 / Chapter 2.4 --- Summary --- p.81 / Chapter Chapter 3 --- Hepatoprotection of Ptr sclerotium --- p.82 / Chapter 3.1 --- Introduction --- p.82 / Chapter 3.1.1 --- Hepatotoxicity --- p.82 / Chapter 3.1.2 --- Potential hepatoprotection effect of Ptr sclerotium --- p.83 / Chapter 3.1.3 --- Toxicity of CC14 --- p.85 / Chapter 3.1.4 --- Toxicity of AFB! --- p.89 / Chapter 3.1.5 --- Bioactivity of chlorophyllin --- p.92 / Chapter 3.1.6 --- Comet assay --- p.93 / Chapter 3.1.7 --- Objectives --- p.98 / Chapter 3.2 --- Materials and Methods --- p.99 / Chapter 3.2.1 --- Sample materials and chemicals --- p.99 / Chapter 3.2.2 --- Curative and preventive tests of Ptr sclerotium against CCl4-induced hepatotoxicity --- p.99 / Chapter 3.2.2.1 --- Animal and diets --- p.99 / Chapter 3.2.2.2 --- Dose-response of CCl4 on rat model --- p.100 / Chapter 3.2.2.3 --- Biochemical assays --- p.100 / Chapter 3.2.2.4 --- Curative hepatoprotection test on Ptr --- p.101 / Chapter 3.2.2.5 --- Preventive hepatoprotection test on Ptr --- p.101 / Chapter 3.2.3 --- Preventive tests of Ptr sclerotium against AFB1-induced hepato- and geno-toxicity --- p.103 / Chapter 3.2.3.1 --- Dose-response of AFB1 on rat model --- p.103 / Chapter 3.2.3.2 --- Preventive test of Ptr against AFB1 --- p.103 / Chapter 3.2.3.3 --- Biochemical assays --- p.105 / Chapter 3.2.3.4 --- Histopathological examination --- p.105 / Chapter 3.2.4 --- Comet assay --- p.106 / Chapter 3.2.4.1 --- Reagent preparations --- p.106 / Chapter 3.2.4.2 --- Procedures --- p.107 / Chapter 3.2.5 --- Statistical analyses --- p.110 / Chapter 3.3 --- Results and Discussion --- p.111 / Chapter 3.3.1 --- Curative and preventive tests of Ptr sclerotium against CCl4-induced hepatotoxicity --- p.112 / Chapter 3.3.1.1 --- Dose-response of CCl4 on rat model --- p.112 / Chapter 3.3.1.2 --- Curative test of Ptr sclerotium against CCl4-induced hepatotoxicity --- p.116 / Chapter 3.3.1.3 --- Preventive test of Ptr sclerotium against CCl4-induced hepatotoxicity --- p.121 / Chapter 3.3.2 --- Preventive tests of Ptr sclerotium against AFB1-induced hepato- and geno-toxicity --- p.126 / Chapter 3.3.2.1 --- Dose-response of AFB1 on rat model --- p.126 / Chapter 3.3.2.2 --- Preventive test of Ptr sclerotium against AFB1-induced geno- and hepatotoxicity --- p.134 / Chapter 3.3.2.3 --- CHL versus 30% Ptr sclerotial diet --- p.137 / Chapter 3.3.3 --- A comparison of the hepatotoxicity of CC14 and AFB1 --- p.142 / Chapter 3.4 --- Summary --- p.147 / Chapter Chapter 4 --- Conclusions and future work --- p.148 / References --- p.151 / Related publication --- p.175

Li Mi. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 125-136). / Abstracts in English and Chinese. / Abstract --- p.i / 論文摘要 --- p.iv / Publications --- p.vi / Acknowledgement --- p.vii / Abbreviations --- p.viii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Pyrrolizidine alkaloids --- p.1 / Chapter 1.1.1 --- Distribution and plant sources --- p.1 / Chapter 1.1.2 --- Structures and nomenclature --- p.3 / Chapter 1.2 --- PA-containing Chinese medicinal herbs --- p.6 / Chapter 1.3 --- PA-induced toxicity。 --- p.7 / Chapter 1.3.1 --- Acute toxicity and chronic toxicity --- p.7 / Chapter 1.3.2 --- Genotoxicity --- p.8 / Chapter 1.3.3 --- Tumorigenicity --- p.8 / Chapter 1.3.4 --- Hepatotoxicity --- p.8 / Chapter 1.3.5 --- Mechanism of toxic effects --- p.9 / Chapter 1.3.5.1 --- Metabolic pathways --- p.10 / Chapter 1.3.5.2 --- Liver tissue-bound pyrroles --- p.16 / Chapter 1.3.5.3 --- Metabolizing enzymes --- p.17 / Chapter 1.3.5.3.1 --- Phase I metabolizing enzymes --- p.17 / Chapter 1.3.5.3.2 --- Phase II metabolizing enzymes --- p.18 / Chapter 1.3.5.4 --- Species and gender specificity toward toxicity --- p.19 / Chapter 1.3.5.5 --- Structure-activity relationships --- p.20 / Chapter 1.4 --- Prevention of PAs-induced toxicity --- p.23 / Chapter 1.4.1 --- Significance of prevention in humans --- p.23 / Chapter 1.4.2 --- Regulations toward preventing toxicity induced by PAs --- p.24 / Chapter 1.5 --- Aim of the present study --- p.25 / Chapter Chapter 2 --- Qualitative and Quantitative Analysis of PA-containing Chinese Medicinal Herbs --- p.26 / Chapter 2.1 --- Materials and equipments --- p.27 / Chapter 2.1.1 --- Herbal materials --- p.27 / Chapter 2.1.2 --- Chemicals and solvents --- p.27 / Chapter 2.1.3 --- Equipment and instrumentation --- p.27 / Chapter 2.2 --- Preparation of herbal extracts。 --- p.28 / Chapter 2.2.1 --- Crude herbal extract --- p.28 / Chapter 2.2.2 --- Total pyrrolizidine alkaloid extract --- p.28 / Chapter 2.3 --- Qualitative and quantitative analysis of Ligularia hodgsonii --- p.29 / Chapter 2.3.1 --- Methods --- p.29 / Chapter 2.3.1.1 --- HPLC-UV condition --- p.29 / Chapter 2.3.1.2 --- HPLC-MS condition --- p.29 / Chapter 2.3.1.3 --- Calibration curve for clivorine --- p.29 / Chapter 2.3.1.4 --- Recovery test --- p.30 / Chapter 2.3.1.5 --- Sample test --- p.30 / Chapter 2.3.2 --- Results and discussions --- p.30 / Chapter 2.3.2.1 --- Qualitative analysis of PAs in Ligularia hodgsonii --- p.30 / Chapter 2.3.2.2 --- Calibration curve for clivorine --- p.35 / Chapter 2.3.2.3 --- Result of the recovery test --- p.37 / Chapter 2.3.2.4 --- Quantification of PAs in Ligularia hodgsonii --- p.37 / Chapter 2.4 --- Qualitative and quantitative analysis of Tussilago farfara --- p.37 / Chapter 2.4.1 --- Methods --- p.38 / Chapter 2.4.1.1 --- HPLC-UV condition --- p.38 / Chapter 2.4.1.2 --- HPLC-MS condition --- p.39 / Chapter 2.4.1.3 --- Calibration curve for senkirkine --- p.39 / Chapter 2.4.1.4 --- Recovery test --- p.39 / Chapter 2.4.1.5 --- Sample test --- p.39 / Chapter 2.4.2 --- Results and discussions --- p.40 / Chapter 2.4.2.1 --- Qualitative analysis of senkirkine in Tussilago farfara --- p.40 / Chapter 2.4.2.2 --- Calibration curve for senkirkine --- p.42 / Chapter 2.4.2.3 --- Result of the recovery test --- p.42 / Chapter 2.4.2.4 --- Quantification of senkirkine in Tussilago farfara --- p.43 / Chapter 2.5 --- Qualitative and quantitative analysis of Gynura segetum --- p.43 / Chapter 2.5.1 --- Methods --- p.43 / Chapter 2.5.1.1 --- HPLC-UV condition --- p.43 / Chapter 2.5.1.2 --- HPLC-MS condition --- p.44 / Chapter 2.5.1.3 --- Calibration curves for senecionine and seneciphylline --- p.44 / Chapter 2.5.1.4 --- Recovery test… --- p.44 / Chapter 2.5.1.5 --- Sample test --- p.44 / Chapter 2.5.2 --- Results and discussions。 --- p.45 / Chapter 2.5.2.1 --- Qualitative analysis of PAs in Gynura segetum --- p.45 / Chapter 2.5.2.2 --- Calibration curves for senecionine and seneciphylline --- p.49 / Chapter 2.5.2.3 --- Result of the recovery test --- p.49 / Chapter 2.5.2.4 --- Quantification of PAs in Gynura segetum --- p.49 / Chapter 2.6 --- Qualitative and quantitative analysis of Crotalaria sessiliflora --- p.50 / Chapter 2.6.1 --- Methods --- p.50 / Chapter 2.6.1.1 --- HPLC-UV condition --- p.50 / Chapter 2.6.1.2 --- HPLC-MS condition --- p.50 / Chapter 2.6.1.3 --- Calibration curve --- p.51 / Chapter 2.6.1.4 --- Recovery test --- p.51 / Chapter 2.6.1.5 --- Sample test --- p.51 / Chapter 2.6.2 --- Results and discussions --- p.52 / Chapter 2.6.2.1 --- Qualitative analysis of monocrotaline in Crotalaria sessiliflora --- p.52 / Chapter 2.6.2.2 --- Calibration curve for monocrotaline --- p.54 / Chapter 2.6.2.3 --- Result of the recovery test --- p.54 / Chapter 2.6.2.4 --- Quantification of PAs in Crotalaria sessiliflora --- p.55 / Chapter 2.7 --- Qualitative and quantitative analysis of Senecio scandens --- p.55 / Chapter 2.7.1 --- Methods --- p.55 / Chapter 2.7.1.1 --- HPLC-UV condition --- p.55 / Chapter 2.7.1.2 --- HPLC-MS condition --- p.56 / Chapter 2.7.1.3 --- Sample test --- p.56 / Chapter 2.7.2 --- Results and discussions --- p.56 / Chapter 2.7.2.1 --- Qualitative analysis of PAs in Senecio scandens --- p.56 / Chapter 2.7.2.2 --- Quantification of PAs in Senecio scandens --- p.59 / Chapter Chapter 3 --- Hepatotoxicity Induced by PA-containing Chinese Medicinal Herbs --- p.60 / Chapter 3.1 --- Materials and methods --- p.62 / Chapter 3.1.1 --- Reagents --- p.62 / Chapter 3.1.2 --- Animal models --- p.62 / Chapter 3.1.3 --- Determination of the serum ALT activity --- p.64 / Chapter 3.1.4 --- Determination of hepatic GSH level --- p.68 / Chapter 3.1.5 --- Quantitation of liver tissue-bound pyrroles --- p.69 / Chapter 3.1.6 --- Histological assessment of liver morphological changes --- p.70 / Chapter 3.1.7 --- Assessment of hepatocytes apoptosis --- p.71 / Chapter 3.1.8 --- Statistical analysis --- p.72 / Chapter 3.2 --- Results and discussion --- p.72 / Chapter 3.2.1 --- Calibration curves --- p.72 / Chapter 3.2.1.1 --- Calibration curve for the determination of serum ALT activity --- p.72 / Chapter 3.2.1.2 --- Calibration curve of determination of hepatic GSH level --- p.73 / Chapter 3.2.2 --- Hepatotoxicity Study of Crotalaria sessiliflora --- p.74 / Chapter 3.2.2.1 --- Hepatotoxicity at 24 hrs after treatment --- p.74 / Chapter 3.2.2.1.1 --- Correlation between dosage of monocrotaline in Crotalaria sessiliflora and amount of liver tissue-bound pyrroles --- p.74 / Chapter 3.2.2.1.2 --- Effects of Crotalaria sessiliflora on the serum ALT activity --- p.79 / Chapter 3.2.2.1.3 --- The correlation between the elevated level of ALT activity and apoptosis of liver cells --- p.85 / Chapter 3.2.2.1.4 --- Effects of Crotalaria sessiliflora on the hepatic GSH level --- p.86 / Chapter 3.2.2.1.5 --- Histological changes of liver sections --- p.89 / Chapter 3.2.2.2 --- Hepatotoxicity within 4 days after administration --- p.92 / Chapter 3.2.2.3 --- Sub-acute hepatotoxicity within 14 days after administration --- p.93 / Chapter 3.2.2.4 --- Conclusion in hepatotoxicity study of Crotalaria sessiliflora --- p.99 / Chapter 3.2.3 --- Hepatotoxicity Study of Gynura segetum --- p.102 / Chapter 3.2.3.1 --- Correlation between the dosage of PAs present in Gynura segetum and the amount of liver tissue-bound pyrroles --- p.102 / Chapter 3.2.3.2 --- "Effects of Gynura segetum on serum ALT activity, hepatic GSH level and morphological changes of liver" --- p.104 / Chapter 3.2.4 --- Hepatotoxicity Study of Ligularia hodgsonii --- p.108 / Chapter 3.2.4.1 --- Correlation between the dosage of PAs present in Ligularia hodgsonii and the formation of liver tissue-bound pyrroles --- p.108 / Chapter 3.2.4.2 --- Effects of Ligularia hodgsonii on serum ALT activity and hepatic GSH level --- p.111 / Chapter 3.2.5 --- Hepatotoxicity Study of Tussilago farfara --- p.113 / Chapter 3.2.6 --- Hepatotoxicity Study of PA-containing medicinal herbs --- p.115 / Chapter 3.2.6.1 --- Correlation between formation of liver tissue-bound pyrroles and elevated serum ALT level --- p.115 / Chapter 3.2.6.2 --- Correlation between dosage of PAs and amount of liver tissue-bound pyrroles --- p.117 / Chapter 3.2.7 --- Test of Liver Tissue-bound Pyrroles as a biomarker using Senecionis scandentis --- p.118 / Chapter 3.2.8 --- Conclusions --- p.120 / Chapter Chapter 4 --- General Conclusions --- p.121 / Chapter 4.1 --- Qualitative and quantitative analysis of five PA-containing medicinal herbs --- p.121 / Chapter 4.2 --- Hepatotoxicity induced by PA-containing medicinal herbs in rats --- p.122 / Chapter 4.3 --- The correlation between hepatotoxicity induced by PA-containing medicinal herbs and the formation of liver tissue-bound pyrroles --- p.123 / Chapter 4.4 --- Threshold of the amount of liver tissue-bound pyrroles related to the hepatotoxicity induced by PA-containing medicinal herbs --- p.123 / References --- p.125

Thesis (Ph. D.)--Ohio State University, 2005. / Title from first page of PDF file. Document formatted into pages; contains xiv, 155 p.; also includes graphics (some col.). Includes bibliographical references (p. 147-155). Available online via OhioLINK's ETD Center

Avasarala Sreedevi. / "December 2004." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (p. 253-272) / 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.

Malgré de nombreux progrès thérapeutiques, la seule réelle option thérapeutique des malades atteints d’une cirrhose terminale ou d’hépatite aiguë fulminante est la transplantation hépatique, cependant limitée par la pénurie d’organes. De même, la prise en charge des pathologies pancréatiques aigues et chroniques consiste essentiellement en traitements supportifs et des complications.<p>La réaction inflammatoire au cours des maladies hépatiques et pancréatiques joue un rôle majeur dans l’évolution de ces maladies car elle influence la sévérité de l’affection aiguë et se complique fréquemment de fibrose et de cirrhose. <p>Les chimiokines constituent une famille de peptides possédant des propriétés chimiotactiques et activatrices sur les leucocytes, et de ce fait jouent un rôle primordial dans la réaction inflammatoire en recrutant des cellules inflammatoires vers un site lésé. Les chimiokines exercent leurs activités en se liant à une famille de récepteurs à 7 hélices transmembranaires situés sur les leucocytes. <p>Le CCR5 est un récepteur pour les chimiokines CCL3 (MIP-1α), CCL4 (MIP-1β), CCL5 (RANTES) et CCL8 (MCP-2). Le CCR5 joue un rôle important de corécepteur dans l’infection par le virus de l’immunodéficience humaine. Chez l’humain, il existe une mutation relativement fréquente du CCR5, appelée CCR5Δ32, qui confère chez les patients homozygotes pour la mutation une protection presque complète contre l’infection par le virus de l’immunodéficience humaine. Plus récemment, la mutation CCR5Δ32 a été rapportée comme étant associée à certaines maladies hépatiques et des traitements expérimentaux chez l’homme par inhibiteurs du CCR5 ont entraînés des cas d’hépatotoxicité sévère. De même, il a été rapporté que l’expression pancréatique de CCR5 était augmentée chez les patients atteints de pancréatite chronique. Cependant, le rôle du récepteur CCR5 et de ses ligands dans la pathogénie des maladies hépatiques et pancréatiques n’est pas connu.<p>Dans un premier temps, nous avons démontré dans un modèle expérimental d’hépatite médiée par les lymphocytes T qu’il existe une production hépatique de CCL3, CCL4 et CCL5 au cours de la maladie et que le foie des souris malades est caractérisé par une infiltration accrue de cellules CCR5+. En utilisant des souris CCR5-déficientes, nous avons ensuite montré que l’absence de CCR5 est associée à une maladie plus sévère, à une production accrue de cytokines pro-inflammatoires et des chimiokines liant le CCR5 (CCL3, CCL4 et CCL5), ainsi que par un recrutement plus important de cellules inflammatoires, particulièrement des cellules CCR1+. Nous avons ensuite montré que la production accrue des ligands du CCR5 joue un rôle important dans l’exacerbation de la maladie observée chez les souris CCR5-déficientes, puisque leur neutralisation réduit fortement la sévérité de la maladie ainsi que le recrutement hépatique de cellules inflammatoires.<p>Dans un second temps, nous avons étudié l’expression et le rôle du CCR5 et de ses ligands dans un modèle murin de pancréatite aiguë sécrétagogue, induite par des injections répétées d’un analogue de la cholécystokinine. Précocément après l’induction de la maladie, nous avons observé une augmentation de l’expression de CCL2 (MCP-1), CCL3 et CCL4 alors que l’augmentation d’expression de CCL5 est observée plus tardivement au cours de la maladie. Nous avons ensuite montré que les souris CCR5-déficientes développent une pancréatite plus sévère, ainsi qu’une production accrue de CCL2, CCL3 et CCL4, et un infiltrat inflammatoire plus marqué que les souris ‘’wild-type’’. Nous avons également montré que la production accrue de ces chimiokines joue un rôle dans l’exacerbation de la pancréatite aiguë chez les souris CCR5-déficientes. En effet, la neutralisation simultanée de ces chimiokines par des anticorps monoclonaux réduit significativement la sévérité de la maladie pancréatique chez ces souris. De même, la neutralisation simultanée des ligands du CCR5 chez des souris wild-type réduit également la sévérité de la pancréatite aiguë, suggérant un rôle de ces molécules dans la pathogénie de la pancréatite aiguë.<p>En conclusion, nous avons montré que l’absence du récepteur CCR5 augmente la susceptibilité aux maladies inflammatoires hépatiques et pancréatiques expérimentales. Le développement d’inhibiteurs du CCR5 dans l’arsenal thérapeutique contre le virus de l’immunodéficience humaine devra tenir compte de ces données, d’autant plus que des cas d’hépatotoxicité sévère ont été récemment rapportés avec certains inhibiteurs en développement et que l’association du virus de l’immunodéficience humaine avec la présence de maladies hépatiques est fréquente. Enfin, ces travaux ouvrent de nouveaux champs d’investigation au niveau de l’étude d’association du CCR5Δ32 avec les maladies inflammatoires pancréatiques et hépatiques, et des perspectives thérapeutiques ciblant CCL3, CCL4 et CCL5. <p><p><p> / Doctorat en sciences médicales / info:eu-repo/semantics/nonPublished

Tissue samples from spotted gar (Lepisosteus oculatus) and largemouth bass (Micropterus salmoides) were collected from Caddo Lake. Gar and bass livers were subjected to histological investigation and color analysis. Liver color (as abs at 400 nm) was significantly correlated with total mercury in the liver (r2 = 0.57, p = 0.02) and muscle (r2 = 0.58, p = 0.01) of gar. Evidence of liver damage as lipofuscin and discoloration was found in both species but only correlated with liver mercury concentration in spotted gar. Inorganic mercury was the predominant form in gar livers. In order to determine the role of mercury speciation in fish liver damage, a laboratory feeding study was employed. Zebrafish (Danio rerio) were fed either a control (0.12 ± 0.002 µg Hg.g-1 dry wt), inorganic mercury (5.03 ± 0.309 µg Hg.g-1 dry wt), or methylmercury (4.11 ± 0.146 µg Hg.g-1 dry wt) diet. After 78 days of feeding, total mercury was highest in the carcass of zebrafish fed methylmercury (12.49 ± 0.369 µg Hg.g-1 dry wt), intermediate in those fed inorganic mercury (1.09 ± 0.117 µg Hg.g-1 dry wt), and lowest in fish fed the control diet (0.48 ± 0.038 µg Hg.g-1 dry wt). Total mercury was highest in the viscera of methylmercury fed zebrafish (11.6 ± 1.86 µg Hg.g-1 dry wt), intermediate in those fed inorganic diets (4.3 ± 1.08 µg Hg.g-1 dry wt), and lowest in the control fish (below limit of detection). Total mercury was negatively associated with fish length and weight in methylmercury fed fish. Condition factor was not associated with total mercury and might not be the best measure of fitness for these fish. No liver pathologies were observed in zebrafish from any treatment.