Physiological responses of yellowtail to fatal environmental hypoxia were compared to those found during Chattonella exposure in normoxia, in order to clarify the roles of blood Po₂ drop in fish kill mechanism by C. marina. Blood Po₂ immediately declined in response to a fall in water Po₂. Most of the measured variables (blood pH, hematocrit, plasma ions, heart rate, blood pressure, ventilatory frequency) did not change until blood Po₂ was decreased to 30-40mm Hg. In contrast, ventilatory pressure was increased at a blood Po₂ of 80mm Hg. Responses in most variables to fatal hypoxia were indistinguishable from those observed when fish were killed by exposure to C. marina. However, plasma chloride concentration was increased to higher levels in fish killed by C. marina than in fish subjected to hypoxia at the lowest blood Po₂ levels, implying dysfunctioning of chloride cells by C. marina. Increases in hematocrit and ventilatory pressure in response to lowered blood Po₂, were attenuated in fish killed by C. marina. Overall, we suspect that the fall in blood Po₂ played a crucial role in fish kill mechanism by C. marina, at least under our experimental conditions, and most other physiological disorders were secondarily brought about by the Po₂ drop.