Effects of two copper compounds on Microcystis aeruginosa cell density, membrane integrity, and microcystin release

•Efficacy of copper sulfate and Cu–EA for controlling M. aeruginosa was different.•Minimum amount of copper required for controlling M. aeruginosa did not cause cell lysis.•Excessive amount of copper could result in cell lysis and greater microcystin release.•Total microcystin concentration would not exceed pretreatment value after treatment.•Degradation of microcystin occurred as copper concentration was 80–1000 µg Cu/L.

Microcystin release following Microcystis aeruginosa cell lysis after copper-based algaecide treatment is often cited as a concern leading to restricted use of algaecide in restoration of natural water resources. To examine this concern, bench-scale experiments were conducted to study responses of M. aeruginosa to 8-day copper exposures as copper sulfate and copper–ethanolamine (Cu–EA). M. aeruginosa UTEX 2385 was cultured in BG11 medium to cell density of 106 cells/mL with total and extracellular microcystin of 93 and 53 μg/L, respectively. Exposures of copper concentration ranged from 40 to 1000 μg Cu/L. Cell membrane integrity was indicated by erythrosine B. In the end of experiment, total microcystin and cell density in untreated control (313 μg/L and 107 cells/mL) was 3.3 and 10 times greater than pretreatment value, respectively. Minimum amount of copper required to reduce M. aeruginosa population within 8 days was 160 μg Cu/L as copper sulfate and 80 μg Cu/L as Cu–EA, where total and extracellular microcystin concentrations (47 and 44 μg/L for copper sulfate; 56 and 44 μg/L for Cu–EA) were degraded with degradation rate coefficient 0.1 day−1 and were less than pretreatment values. Given a copper concentration at 80 µg Cu/L as Cu–EA, M. aeruginosa cells were intact and less microcystin were released compared to treatments at 160–1000 µg Cu/L, where lysed cells and relatively greater microcystin release were observed. Based on the laboratory results, a minimum amount of copper required for reducing M. aeruginosa population could decrease total microcystin concentration and not compromise cells and minimize microcystin release.

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