RELEASE AND DEGRADATION OF MICROCYSTIN FOLLOWING ALGICIDE TREATMENT OF A MICROCYSTIS-AERUGINOSA BLOOM IN A RECREATIONAL LAKE, AS DETERMINED BY HPLC AND PROTEIN PHOSPHATASE INHIBITION ASSAY

Algicide treatment of an hepatotoxic Microcystis aeruginosa Kuetzing emend. Elenkin bloom on Lake Centenary caused cell lysis and the release of microcystin into the surrounding water. Where M. aeruginosa was confined to accumulations along the leeward shore of the lake, dissolved microcystin was detected for only 24 hours after spraying. It was presumed that the toxin was rapidly diluted by uncontaminated water from the main body of the lake. At an enclosed site in the south-west corner of the lake, microcystin persisted at high levels (1300-1800 mu gl(-1)) for 9 days before degradation commenced. Microcystin degradation kinetics following this 9 day lag phase were bi-phasic with a rapid phase lasting 3 days (90-95% loss), and a slower phase which continued until a flash flood on day 21. HPLC analysis and protein phosphatase assay revealed the same overall trend of microcystin release, persistence and then degradation. However, there was a rapid increase in protein phosphatase inhibition from day 5 to day 9 before degradation commenced. These results suggest that the initial bacterial transformation of microcystin resulted in a product more inhibitory to protein phosphatase than the parent toxin.