The effect of nutrient levels and ratios on the growth of Microcystis aeruginosa and microcystin production
- Authors: Sember, Craig Stewart
- Date: 2002
- Subjects: Microcystis aeruginosa -- Toxicology , Nitrates , Microcystins
- Language: English
- Type: Thesis , Masters , MSc
- Identifier: vital:11076 , http://hdl.handle.net/10948/287 , Microcystis aeruginosa -- Toxicology , Nitrates , Microcystins
- Description: This study reports the findings on the effect of nitrates and phosphates on the biomass and toxin production of various strains of the unicellular non-nitrogen fixing cyanobacterium, Microcystis aeruginosa. The occurrence of blooms of Microcystis aeruginosa and microcystin in freshwater impoundments across the globe has been on the increase lately due to increased levels of eutrophication, resulting in human and animal deaths and illness, as well as drinking and recreational water foulment. A range of environmental factors have been shown to effect growth and microcystin production. Existing literature however is somewhat contradictory as to the effects of these physical and chemical factors on toxin production. Therefore Microcystis aeruginosa strains were cultured under batch and continuous conditions to determine the effect of nitrate and phosphate concentrations and ratios on biomass and toxin production. Cultures were analysed with regards to internal nutrient stores, biomass production, nutrient depletion, photosynthetic efficiency and microcystin production. Results showed that microcystin production correlated to growth rate, photosynthetic efficiency and internal nitrogen stores and that an optimal N:P ratio was associated with microcystin levels, growth rate and photosynthetic efficiency. Results therefore led to the conclusion that the nitrogen, carbon, and phosphate balance within the cell is closely associated with microcystin production. Whether or not microcystin is produced to maintain this balance or produced as a function of this balance remains to be determined.
- Full Text:
- Date Issued: 2002
- Authors: Sember, Craig Stewart
- Date: 2002
- Subjects: Microcystis aeruginosa -- Toxicology , Nitrates , Microcystins
- Language: English
- Type: Thesis , Masters , MSc
- Identifier: vital:11076 , http://hdl.handle.net/10948/287 , Microcystis aeruginosa -- Toxicology , Nitrates , Microcystins
- Description: This study reports the findings on the effect of nitrates and phosphates on the biomass and toxin production of various strains of the unicellular non-nitrogen fixing cyanobacterium, Microcystis aeruginosa. The occurrence of blooms of Microcystis aeruginosa and microcystin in freshwater impoundments across the globe has been on the increase lately due to increased levels of eutrophication, resulting in human and animal deaths and illness, as well as drinking and recreational water foulment. A range of environmental factors have been shown to effect growth and microcystin production. Existing literature however is somewhat contradictory as to the effects of these physical and chemical factors on toxin production. Therefore Microcystis aeruginosa strains were cultured under batch and continuous conditions to determine the effect of nitrate and phosphate concentrations and ratios on biomass and toxin production. Cultures were analysed with regards to internal nutrient stores, biomass production, nutrient depletion, photosynthetic efficiency and microcystin production. Results showed that microcystin production correlated to growth rate, photosynthetic efficiency and internal nitrogen stores and that an optimal N:P ratio was associated with microcystin levels, growth rate and photosynthetic efficiency. Results therefore led to the conclusion that the nitrogen, carbon, and phosphate balance within the cell is closely associated with microcystin production. Whether or not microcystin is produced to maintain this balance or produced as a function of this balance remains to be determined.
- Full Text:
- Date Issued: 2002
The effect of selenium in the detoxification of the microcystin hepatotoxins
- Authors: Downs, Kerry
- Date: 2002
- Subjects: Cynaobacterial toxins , Microcystins , Selenium
- Language: English
- Type: Thesis , Masters , MSc
- Identifier: vital:11070 , http://hdl.handle.net/10948/284 , Cynaobacterial toxins , Microcystins , Selenium
- Description: Blooms of cyanobacteria have been known to cause illness in humans and death in wild and domestic animals. One of the toxins produced by cyanobacteria is microcystin, which is a potent hepatotoxin. Microcystin is taken up by bile acid transporters in the intestine and transported into the liver. After exposure to acute doses of microcystin, severe haemorrhage has been observed along with apoptotic and necrotic hepatocytes. The cytoskeletal structure of the hepatocytes is disrupted and oxidative stress is induced. Selenium, a known anti-oxidant, has been shown to induce increased activity of glutathione peroxidase. Glutathione peroxidase removes peroxides from cells protecting them from oxidative stress. This study set out to determine if selenium could play a role in preventing the damage to mice livers due to microcystin toxin. The protective role of selenium was explored in three main studies: in the first study, the ability of selenium to increase the survival time of mice exposed to a lethal dose of toxin was determined. In the second study the mice were exposed to sublethal chronic doses of toxin over 30 days. The ability of selenium to minimise liver damage under these conditions was determined. The final study investigated the mechanism of the protective effect of selenium. The results of the first study suggested that selenium could extend survival time. In the second study the selenium supplemented mice showed a reduction in the extent of the increase in liver weight and a decrease in the amount of lipid peroxidation induced compared to the mice that received only toxin. The histology of the selenium supplemented mice also showed a decrease in the severity and amount of morphological changes in the liver. The third study indicated that the protection shown by selenium might be mediated by an increase in the glutathione peroxidase (GPX) activity in selenium supplemented mice. This increase in GPX activity would increase the removal of the lipid hydroperoxides and prevent the damage they would cause in the cell. A further result indicated an increase in glutathione S-transferase in only the toxin control mice when compared to the selenium supplemented and control mice. ii In conclusion selenium offers protection against microcystin but further studies need to be done to provide statistically valid results to clarify the level of protection.
- Full Text:
- Date Issued: 2002
- Authors: Downs, Kerry
- Date: 2002
- Subjects: Cynaobacterial toxins , Microcystins , Selenium
- Language: English
- Type: Thesis , Masters , MSc
- Identifier: vital:11070 , http://hdl.handle.net/10948/284 , Cynaobacterial toxins , Microcystins , Selenium
- Description: Blooms of cyanobacteria have been known to cause illness in humans and death in wild and domestic animals. One of the toxins produced by cyanobacteria is microcystin, which is a potent hepatotoxin. Microcystin is taken up by bile acid transporters in the intestine and transported into the liver. After exposure to acute doses of microcystin, severe haemorrhage has been observed along with apoptotic and necrotic hepatocytes. The cytoskeletal structure of the hepatocytes is disrupted and oxidative stress is induced. Selenium, a known anti-oxidant, has been shown to induce increased activity of glutathione peroxidase. Glutathione peroxidase removes peroxides from cells protecting them from oxidative stress. This study set out to determine if selenium could play a role in preventing the damage to mice livers due to microcystin toxin. The protective role of selenium was explored in three main studies: in the first study, the ability of selenium to increase the survival time of mice exposed to a lethal dose of toxin was determined. In the second study the mice were exposed to sublethal chronic doses of toxin over 30 days. The ability of selenium to minimise liver damage under these conditions was determined. The final study investigated the mechanism of the protective effect of selenium. The results of the first study suggested that selenium could extend survival time. In the second study the selenium supplemented mice showed a reduction in the extent of the increase in liver weight and a decrease in the amount of lipid peroxidation induced compared to the mice that received only toxin. The histology of the selenium supplemented mice also showed a decrease in the severity and amount of morphological changes in the liver. The third study indicated that the protection shown by selenium might be mediated by an increase in the glutathione peroxidase (GPX) activity in selenium supplemented mice. This increase in GPX activity would increase the removal of the lipid hydroperoxides and prevent the damage they would cause in the cell. A further result indicated an increase in glutathione S-transferase in only the toxin control mice when compared to the selenium supplemented and control mice. ii In conclusion selenium offers protection against microcystin but further studies need to be done to provide statistically valid results to clarify the level of protection.
- Full Text:
- Date Issued: 2002
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