Antioxidant responses and degradation of two antibiotic contaminants in Microcystis aeruginosa

Cyanobacteria may interact with antibiotic contaminants in aquatic environments, but the interaction effects and mechanisms remain unclear. In the present study, aqueous culture of Microcystis aeruginosa was exposed to 50 ng/l–1 μg/l of spiramycin and amoxicillin for seven days. The influences of antibiotics on the antioxidant system of M. aeruginosa and the degradation of antibiotics by M. aeruginosa were investigated. The activities of superoxide dismutase (SOD) in spiramycin-treated M. aeruginosa were stimulated by up to 2.2 folds, while the activities of peroxidase (POD) and catalase (CAT) were inhibited by spiramycin at test concentrations of 500 ng/l–1 μg/l, with a decrease of up to 71% and 76% compared to the control, respectively. The activities of SOD, POD and CAT in M. aeruginosa were stimulated by amoxicillin during the whole exposure period, with respective increases of up to 60%, 30% and 120% relative to the control. At test concentrations of 500 ng/l–1 μg/l, the higher MDA contents in spiramycin-treated M. aeruginosa indicated a higher toxicity of spiramycin than amoxicillin, possibly due to the accumulation of hydrogen peroxide caused by the inhibited activities of POD and CAT under exposure to spiramycin. The increase of glutathione content, the stimulation of glutathione S-transferase activity and the degradation of each antibiotic were observed in M. aeruginosa during the 7-day exposure. At the end of exposure, 12.5%–32.9% of spiramycin and 30.5%–33.6% of amoxicillin could be degraded by M. aeruginosa from the culture medium, indicating the ability of M. aeruginosa to eliminate coexisting contaminants via detoxification.

► Antioxidant responses of Microcystis aeruginosa to two antibiotics were observed.
► Spiramycin and amoxicillin affected the elimination of H2O2 in different manners.
► 12.5%–32.9% of spiramycin and 30.5%–33.6% of amoxicillin were degraded by this alga.
► Glutathione conjugation was a possible pathway for the biodegradation of antibiotics.