Over the last several decades, harmful algal blooms (HABs) have emerged as a global environmental problem because of their more frequent occurrence and because of the threat they pose to the health of humans and other organisms. Great efforts have been made to elucidate the ecological and biological features of red tide events, using approaches ranging from molecular and cell biology to large-scale field surveys, numerical modeling, and remote sensing from space. However, studies on the molecular mechanisms of red tides, including those involved in their decline phase, are still limited. Researchers believe that the decline phase of red tides represents a process of programmed cell death (PCD). PCD, which is controlled by multiple factors, is an active, gene-regulated process that has evolved in most organisms. Alexandrium catenella is an important causative dinoflagellate associated with HABs and paralytic shellfish poisoning. In this study, we determined physiological and biochemical indices of A. catanella including soluble protein content, superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, reduced glutathione (GSH) content, hydrogen peroxide (H₂O₂) content, photosynthetic rate, respiratory rate, DNA laddering, and telomerase activity. These biochemical analyses were conducted using cells of A. catenella collected after different periods of growth and under different growth conditions (i.e., with different concentrations of nitrogen in the medium). There were differences in several parameters between the decline phase and the logarithmic phase. There was an increase in peroxidation in A. catenella during the decline phase and under low-and high-nitrogen conditions. This was characterized by increased SOD activity (except under low-nitrogen growth conditions), MDA content, and H₂O₂ content, and decreases in soluble protein content, GSH content, photosynthetic rate, and respiratory rate. The results suggested that excessive reactive oxygen was the main reason for the decline of A. catenella. Based on these experimental results, we hypothesized that the physiological process during the decline phase of A. catenella was as follows: First, metabolism slowed, resulting in a decrease in intracellular protein levels. Secondly, cells produced large amounts of peroxide, which activated the cellular antioxidant system. SOD was activated in response to the massive accumulation of ROS, and other non-enzymatic antioxidants such as GSH were consumed. In spite of these changes, the oxidation and antioxidant system remained unbalanced, resulting in excess accumulation of H₂O₂ and other ROS. Ultimately, those ROS led to serious membrane lipid peroxidation and the release of MDA. The decrease in SOD activity under low-nitrogen conditions may have been due to a lack of nitrogen, which is necessary for protein synthesis. Finally, excessive accumulation of ROS induced apoptosis, and the endonuclease was activated to selectively degrade chromosomes, resulting in DNA laddering. The photosynthetic rate decreased as a result of decreases in chlorophyll content and RUBP carboxylase activity. The respiration rate decreased as a result of the decreased volume of mitochondria and smaller area of their internal cristae. Telomerase activity also changed during the cell growth and decline periods. Low-nitrogen and high-nitrogen conditions accelerated the physiological process of cell aging. These results are consistent with the hypothesis that the decline of A. catenella is a controlled process of cell death. Our findings reveal some of the physiological changes that occur during the decline phase of A. catenella. These data will help us to understand the decline mechanisms of red tide algae, and provide a foundation for studying the molecular mechanisms of red tide dynamics. Such information will be useful for developing methods to monitor and control red tides.