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A Chrysophyceae species, Poterioochromonas sp., was isolated from Microcystis cultures. This species can efficiently prey on Microcystis and can grow faster phagotrophically than autotrophically. The growth of Poterioochromonas sp. was stimulated in the presence of microcystin-LR and microcystin-RR (in concentrations ranging from 0.1 to 4 mg/L). The growth rate of Poterioochromonas was 45 times higher than the control, indicating the toxins serve as growth stimuli for this organism. A subculture of toxin-treated cells, however, showed low cellular viability, suggesting that growth enhancement by microcystins was not a normal process. The antioxidant enzymatic activity of Poterioochromonas sp. was screened for toxicology analysis. Glutathione, malondialdehyde, and superoxide dismutase (SOD) content was up-regulated within 8 h of exposure to microcystin-LR (500 g/L). A high level of SOD activity during exposure to the toxin indicated that SOD was involved in decreasing oxidative stress caused by microcystin-LR. Simultaneously with growth, Poterioochromonas was able to degrade microcystin-LR even, at a toxin concentration of 4 mg/L. This putative degradation mechanism in Poterioochromonas is explored further and discussed in this article. Our findings may shed light on understanding the role of Poterioochromonas in the aquatic ecosystem, in particular, as a grazer of toxic cyanobacteria and a biodegrader for microcystins. 2005 Wiley Periodicals, Inc. Environ Toxicol 20: 373380, 2005. [ABSTRACT FROM AUTHOR]

In the current study, the toxicological mechanisms of microcystin-LR and its disadvantageous effects on Daphnia magna were examined. Survival rate, number of newborn, activity of several important enzymes [glutathione S-transferase (GST), lactate dehydrogenase (LDH), phosphatases, and glutathione], accumulated microcystins, and ultrastructural changes in different organs of Daphnia were monitored over the course of 21-day chronic tests. The results indicated that low concentrations of dissolved microcystin had no harmful effect on Daphnia. On the contrary, stimulatory effects were detected. In the presence of toxin at high dosage and for long-term exposure, GST and glutathione levels decreased significantly. The decreased enzyme activity in the antioxidant system probably was caused by detoxification reactions with toxins. And these processes of detoxification at the beginning of chronic tests may enable phosphatases in Daphnia magna to withstand inhibition by the toxins. At the same time, we also found that the LDH activity in test animals increased with exposure to microcystin-LR, indicating that adverse effects occurred in Daphnia. With microcystin given at a higher dosage or for a longer exposure, the effect on Daphnia magna was fatal. In the meantime, microcystin began to accumulate in Daphnia magna, and phosphatase activity started to be inhibited. From the ultrastructure results of cells in D. magna, we obtained new information: the alimentary canal may be the target organ affected by exposure of microcystins to D. magna. The results of the current study also suggested that the oxidative damage and PPI (protein phosphatase inhibition) mechanisms of vertebrates also are adapted to Daphnia. 2005 Wiley Periodicals, Inc. Environ Toxicol 20: 323330, 2005. [ABSTRACT FROM AUTHOR]