Microcystin interferes with defense against high oxidative stress in harmful cyanobacteria

Abstract Harmful cyanobacteria producing toxic microcystins are a major concern in water quality management. In recent years, hydrogen peroxide (H 2 O 2 ) has been successfully applied to suppress cyanobacterial blooms in lakes. Physiological studies, however, indicate that microcystin protects cyanobacteria against oxidative stress, suggesting that H 2 O 2 addition might provide a selective advantage for microcystin-producing (toxic) strains. This study compares the response of a toxic Microcystis strain, its non-toxic mutant, and a naturally non-toxic Microcystis strain to H 2 O 2 addition representative of lake treatments. All three strains initially ceased growth upon H 2 O 2 addition. Contrary to expectation, the non-toxic strain and non-toxic mutant rapidly degraded the added H 2 O 2 and subsequently recovered, whereas the toxic strain did not degrade H 2 O 2 and did not recover. Experimental catalase addition enabled recovery of the toxic strain, demonstrating that rapid H 2 O 2 degradation is indeed essential for cyanobacterial survival. Interestingly, prior to H 2 O 2 addition, gene expression of a thioredoxin and peroxiredoxin was much lower in the toxic strain than in its non-toxic mutant. Thioredoxin and peroxiredoxin are both involved in H 2 O 2 degradation, and microcystin may potentially suppress their activity. These results show that microcystin-producing strains are less prepared for high levels of oxidative stress, and are therefore hit harder by H 2 O 2 addition than non-toxic strains.