Microcystin enhances the fitness of microcystin producing cyanobacteria at high light intensities by either preventing or retarding photoinhibition
- Authors: Phelan, Richard Reginald
- Date: 2013
- Subjects: Microcystins , Microcystis , Cyanobacterial toxins
- Language: English
- Type: Thesis , Doctoral , PhD
- Identifier: vital:10354 , http://hdl.handle.net/10948/d1020957
- Description: Several genera of cyanobacteria produce microcystin, a monocyclic peptide, with a unique chemical structure. To date, there have been over a 100 different structural variants of microcystin which have been identified. Microcystin production is affected by numerous environmental factors. However, the primary modulating factor for intracellular microcystin quota is the intracellular N:C ratio. No clearly defined biological role has been described for microcystin. Proposed roles for microcystin include defence against plankton grazers, metal chelation, an infochemical and a protectant against oxidative stress. There is sufficient evidence to support a biological role for microcystin in photosynthesis: microcystin is predominantly located in the thylakoid membranes, the microcystin gene cluster is differentially expressed as a function of light and a growth advantage for the microcystin producer in saturating light intensities. The purpose of this study is to investigate a possible biological role for microcystin in preventing photoinhibition and thus explaining the growth advantage observed in toxin-producers over non-toxin-producers. The uptake of exogenous microcystin was observed in Synechocystis PCC 6803 which was internalized and located in the thylakoid membranes and caused the inhibition of photosynthesis. Microcystin variants and increasing concentrations of microcystin-LR had no effect on the fluidity of the thylakoid membranes. The exposure of thylakoid membranes from Synechocystis PCC 6803 to physiologically relevant concentrations of different microcystin variants resulted in the inhibition of photosystem II activity but not photosystem I activity. The inhibition of photosystem II was variant dependent and concentration dependent for microcystin-LR and microcystin-RR. Chlorophyll a fluorescence data showed that photosystem II inhibition was caused by the inhibition of the oxygen evolving complex. Furthermore, a completion study revealed that the microcystin-producing Microcystis PCC 7806 had a competitive advantage over the non-microcystin producing ΔmcyA mutant of Microcystis PCC 7806 at high light intensities. The data indicates that microcystin protects the toxin-producer by either retarding or preventing photoinhibition and thus identifying the first data supported function for microcystin in cyanobacteria.
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- Date Issued: 2013
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.
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- 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.
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- Date Issued: 2002