Influences of small-scale oscillations on growth inhibition and ultrastructural changes of Microcystis cells.

We investigated the effects of small-scale oscillation (SSO) on toxic Microcystis cells. The oscillating device was made of silicon with two axes that had a diameter of ∼40 mm, and a frequency of 2.5 Hz was observed at 150 rpm. The SSO was effective in inhibiting Microcystis growth. Microcystin release was not observed, whereas cell density barely increased in the oscillating group. Cell size and morphology of the oscillating group were no different from the control group. However, cell quotas of chl.a and microcystin in the oscillating group were half the level of the control group. Crucially, a number of large-sized holes were observed and layered long linear thylakoids were rarely observed in the oscillating group. Therefore, SSO was found to be very effective in Microcystis growth inhibition, and it caused ultrastructural changes without damage to the cell membrane and subsequent microcystin release.

Microcystin release and Microcystis cell damage mechanism by alum treatment with long-term and large dose as in-lake treatment.

Most of our previous studies reported aluminum causes no cell damage or lysis, and no subsequent toxin release in conventional treatment of drinking water or in the laboratory, on the contrary, we investigated the effect of long-term and large-dose alum treatment, because the environmental conditions in lakes and treatment plants are widely different. The microcosm experiments were designed to simulate the effect of adding alum under the similar conditions of common lakes and reservoirs, and the bottle experiments were conducted to examine the budget or dynamics of microcystin after adding alum. In precipitate analyses, we also confirm the release and dynamics of microcystin and the damage mechanisms of Microcystis cells under alum treatment. In microcosms treated with alum alone, the extracellular microcystin-LR (MC-LR) concentration increased to approximately 82% in 7 days. Similar results were obtained in bottle experiments. By plotting the concentration of released microcystin over time, we inferred that the extracellular MC-LR concentration exponentially rose toward an asymptotic maximum. Moreover, in scanning electron microscope images, some cells exhibited torn membranes with miniscule traces of aluminum hydroxide coating. We conclude that alum treatment, particularly at maximum dosage administered over long periods, seriously damages Microcystis cells and induces microcystin release. Therefore, long-term application of large alum doses is not recommended as an in-lake treatment.

The removal of Microcystis ichthyoblabe cells and its hepatotoxin microcystin-LR during electrooxidation process using Pt/Ti electrodes.

Electrooxidation is widely used to remove harmful organic and inorganic substances as well as pathogenic microorganisms. This study investigates the removal of Microcystis ichthyoblabe cells and their hepatotoxin microcystin-LR by the electrooxidation process using Pt/Ti electrodes. Additionally, the morphology changes and cell sizes were determined by scanning electron microscopy and a particle size analyzer, respectively. The algal cells were severely damaged by the electrooxidation process. During the initial treatment, intracellular microcystin-LR was released from the cells, increasing the extracellular microcystin-LR concentration. The electrooxidation charge required to remove cells and MC-LR was 3 × 10(4) C and 6 × 10(4) C, respectively. The removal efficiencies of M. ichthyoblabe cells and microcystin-LR were insensitive to initial cell density, initial microcystin-LR concentration and solution conductivity, but were heavily reduced at large algal suspension volume. Therefore, to achieve simultaneous removal of Microcystis cells and their MC, it is necessary to control the volume of algal suspension.

Detoxification of microcystin-LR in water by Portulaca oleracea cv.

Microcystin-LR (0.02 µg/ml) in the hydroculture medium of Portulaca oleracea cv., became below the detection level (<0.0001 µg/ml) by HPLC analysis after 7 days. The toxicity of microcystin estimated with protein phosphatase inhibition assay, however, remained at 37% of the initial level, indicating that microcystin-LR was transformed by P. oleracea cv. into unknown compound(s) of lower toxicity.

The effect of alum coagulation for in-lake treatment of toxic Microcystis and other cyanobacteria related organisms in microcosm experiments.

Microcosm and bottle experiments were conducted to evaluate the effects of alum treatment on cyanobacteria-lysing organisms and microcystin-degrading bacteria as well as Microcystis cells, and to provide detailed evidence of Microcystis cell damage by investigating precipitated Microcystis cells. The alum concentration to be pH 6.0 is the maximum which does not cause toxicity by monomeric Al, therefore, this concentration was defined as maximum dose. Microcystis cells were considerably damaged by the alum treatment with maximum dose and long contact time. Seven days post-treatment, intracellular microcystin-LR was released into the extracellular environment in excess of 95 percent and chlorophyll a is not easily released from inside the cell, chl.a of precipitated Microcystis cells was also decreased to approximately 50 percent. Moreover, alum treatment caused damage to cyanobacteria-lysing organisms and microcystin-degrading bacteria, as well as to Microcystis cells. Therefore, it could be concluded that alum treatment with maximum dose (48 mg L(-1) as AI) is not suitable for removing cyanobacterial bloom without the release of cyanotoxin in reservoirs and ponds.