Thesis (Ph. D.)--University of Florida, 2006. / Title from title page of source document. Document formatted into pages; contains 119 pages. Includes vita. Includes bibliographical references.

Thesis (Ph.D.)--University of Nebraska-Lincoln, 2006. / Title from title screen (site viewed on Nov. 10, 2006). PDF text: v, 131 p. : ill. ; 0.77Mb. UMI publication number: AAT 3216104. Includes bibliographical references. Also available in microfilm and microfiche format.

Thesis (Ph. D.)--University of Texas at Austin, 2005. / Vita. Includes bibliographical references.

Thesis (Ph. D.)--University of Canterbury, 2006. / Typescript (photocopy). Includes bibliographical references. Also available via the World Wide Web.

Nitrification is the conversion of ammonia to nitrate via nitrite and is performed by ammonia oxidising archaea (AOA), complete ammonia-oxidiser (comammox) and ammonia and nitrite oxidising bacteria (AOB and NOB). The aim of this study is to examine the effect of ammonia concentration, temperature, drought and inhibitors on activity of AOA and AOB using soil microcosms and cultures. Ammonia concentration in soil increases during drought due to the reduced soil water content and, with desiccation stress or a combination of both factors, may result in reported greater inhibition of AOA than AOB during drought. The independent effects of both matric potential and initial ammonium concentration on AOA and AOB amoA abundances and nitrate production were studied in soil microcosms. AOA were more susceptible to increased desiccation stress than AOB, irrespective of initial soil ammonium concentration, and AOA cultures were more sensitive than AOB to osmotic stress induced by different concentrations of NaCl or sorbitol. This may represent an additional niche differentiating factor between AOA and AOB in soil. The effect of temperature and supply of high levels of inorganic ammonium on ammonia oxidation by AOA and AOB were also investigated in soil microcosms. Activity and growth of AOA and AOB were observed in soil amended with high ammonium concentration with increasing temperature, suggesting that AOA can contribute to nitrification in highly fertilised soil, particularly at 25 oC. Inhibition of AOA by simvastatin was investigated in culture and in soil. Simvastatin selectively inhibited AOA in both systems and soil microcosm studies provided evidence for oxidation of ammonia by AOB at low ammonium concentration. Generally, the results show the benefits of combining soil microcosm and culture-based approaches in soil microbiology. The findings advance our understanding of the influence of ammonium supply, temperature and osmotic stress on soil nitrification and its role in controlling the availability of ammonium-based fertilisers for plant uptake.

The aim of the work presented in this thesis was to assess the protective properties of the bioflavanoid drug, (+)-catechin, and its palmityl ester, 3-palmitoyl-(+)-catechin, against ethanol hepato-toxicity (ie: fatty liver) in the rat. In initial experiments, both (+)-catechin compounds were found to protect against the hepatic lipid accumulation (mainly triglyceride) after acute ethanol dosing, and after long-term feeding of ethanol in a liquid diet. In the latter situation, 3-palmitoyl-(+)-catechin was significantly more effective than (+)-catechin itself at preventing fatty liver, probably as a result of its greater lipid solubility and longer half-life in the liver tissue. Published work suggested two possible mechanisms of action for the (+)-catechin compounds against ethanol hepatotoxicity. Firstly, the ability of the drugs to correct the elevated hepatic NADH:NAD ratio (redox-state) after ethanol dosing may limit steatosis. Secondly, free radical scavenging properties may prevent liver injury occurring as a result of ethanol-induced lipid peroxidation. Acute experiments were performed which confirmed that the (+)-catechin compounds corrected the redox-state change after acute ethanol administration, but subsequent studies in which correction of the redox-state by Naloxone or Methylene Blue was found to have little influence on ethanol-induced steatosis, suggested that this was not the mechanism of action of the drugs. Synthetic antioxidants (free radical scavengers) were found to prevent both acute and chronic ethanol-induced fatty liver, under the same experimental conditions as those under which the (+)-catechin compounds afforded protection, without reversing the redox-state change after ethanol dosing. 3-Palmitoyl-(+)-catechin was then shown to prevent ethanol-induced hepatic lipid peroxidation (measured as mitochondrial diene conjugates and liver malonaldehyde levels) after acute ethanol dosing, at the same time as preventing triglyceride accumulation. As other effects of the compounds which might influence fat accumulation after ethanol were excluded (eg: inhibition of ethanol metabolism or lowering of liver acetaldehyde concentrations), it was concluded that the (+)-catechin compounds protect against alcoholic fatty liver in rats by inhibiting ethanol-induced lipid peroxidation, and the possible consequence of the latter (ie: mitochondrial damage and impaired fatty acid oxidation), rather than acting through modulation of the redox-state. The findings here cast doubts on the commonly-quoted 'redox-state' mechanism for fatty liver production by ethanol, and support the lipid peroxidation hypothesis for alcoholic liver injury.

No description available.

No description available.

No description available.

No description available.