EFFECT OF ELEVATED TEMPERATURE, DARKNESS, AND HYDROGEN PEROXIDE TREATMENT ON OXIDATIVE STRESS AND CELL DEATH IN THE BLOOM‐FORMING TOXIC CYANOBACTERIUM <i>MICROCYSTIS AERUGINOSA</i>¹

<jats:p>This study assessed the implication of oxidative stress in the mortality of cells of <jats:italic>Microcystis aeruginosa</jats:italic> Kütz. Cultures grown at 25°C were exposed to 32°C, darkness, and hydrogen peroxide (0.5 mM) for 96 h. The cellular abundance, chl <jats:italic>a</jats:italic> concentration and content, maximum photochemical efficiency of PSII (<jats:italic>F</jats:italic><jats:sub>v</jats:sub>/<jats:italic>F</jats:italic><jats:sub>m</jats:sub> ratio), intracellular oxidative stress (determined with dihydrorhodamine 123 [DHR]), cell mortality (revealed by SYTOX‐labeling of DNA), and activation of caspase 3–like proteins were assessed every 24 h. The presence of DNA degradation in cells of <jats:italic>M. aeruginosa</jats:italic> was also assessed using a terminal deoxynucletidyl transferase‐mediated dUTP nick end labeling (TUNEL) assay at 96 h. Transferring cultures from 25°C to 32°C was generally beneficial to the cells. The cellular abundance and chl <jats:italic>a</jats:italic> concentration increased, and the mortality remained low (except for a transient burst at 72 h) as did the oxidative stress. In darkness, cells did not divide, and the <jats:italic>F</jats:italic><jats:sub>v</jats:sub>/<jats:italic>F</jats:italic><jats:sub>m</jats:sub> continuously decreased with time. The slow increase in intracellular oxidative stress coincided with the activation of caspase 3–like proteins and a 15% and 17% increase in mortality and TUNEL‐positive cells, respectively. Exposure to hydrogen peroxide had the most detrimental effect on cells as growth ceased and the <jats:italic>F</jats:italic><jats:sub>v</jats:sub>/<jats:italic>F</jats:italic><jats:sub>m</jats:sub> declined to near zero in less than 24 h. The 2‐fold increase in oxidative stress matched the activation of caspase 3–like proteins and a 40% and 37% increase in mortality and TUNEL‐positive cells, respectively. These results demonstrate the implication of oxidative stress in the stress response and mortality of <jats:italic>M. aeruginosa.</jats:italic></jats:p>