Cyanotoxin impact on microbial-mediated nitrogen transformations at the interface of sediment-water column in surface water bodies
2020
Li, Hanyan | Hollstein, Marielle | Podder, Aditi | Gupta, Vedansh | Barber, Michael | Goel, Ramesh
Harmful cyanobacterial blooms produce lethal toxins in many aquatic ecosystems experiencing eutrophication. This manuscript presents results on the effects of cyanotoxins on the aerobic microbial communities residing at the interface of sediments and water columns with the ammonia-oxidizing bacteria (AOB) as the model microbial community. Microcystin-LR (MC-LR), a heavily researched cyanotoxin variant, was used as the model cyanotoxin. To measure cyanotoxin influence on the activity of nitrifying microbial communities, an enriched culture of AOBs collected from an ongoing partial nitrification-nitritation reactor was examined for its exposure to 1, 5 and 10 μg/L of MC-LR. The nitritation kinetics experiment demonstrated MC-LR’s ability at 1, 5, and 10 μg/L concentrations to prevent ammonium oxidation with statistically significant differences in nitritation rates between the blanks and spiked samples (One-way ANOVA, p < 0.05). Significantly decreased dissolved oxygen (DO) consumption during oxygen update batch tests demonstrated toxin’s influence on AOB’s oxidizing capabilities when exposed to even lower concentrations of 0.75, 0.5, and 0.25 μg/L of MC-LR in a separate set of experiments. Based on competitive kinetics, the MC-LR inhibition coefficient-the concentration needed to produce half-maximum inhibition of the mixed community AOBs was determined to be 0.083 μg/L. The stress tests proved the recovery of nitritation to some extent at lower MC-LR concentrations (1 and 5 μg/L), but significant irreversible inhibition was recorded when the AOB population was exposed to 10 μg/L MC-LR. The comparisons of amoA gene expressions corresponded well with nitrifying kinetics. All concentrations of MC-LR spiking were determined to produce a discernible impact on the AOB nitritation rate by either destroying the bacterial cell or immediately inhibiting the amoA gene expression.
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