Unravelling the pathway of respiratory toxicity in goldlined seabream (Rhabdosargus sarba) induced by the harmful alga Chattonella marina.

The harmful alga Chattonella marina has caused massive fish kills and economic losses worldwide. Suffocation is generally believed to be the major cause of fish death by C. marina. However, the specific mechanisms leading to respiratory disorder in fish and subsequent fish kills by C. marina remain unknown. The goldlined seabream, highly susceptible to C. marina, was employed to investigate temporal changes of physiological, histopathological and biochemical parameters related to respiratory function at different stages of exposure to C. marina. Hemoglobin oxidation and blood lyses were not found in goldlined seabream exposed to C. marina, which could not be the key reasons accounting for pO(2) drop in the stressed fish. Gill histopathology such as irregular organization of lamellae, mucous with algal cells trapped in interfilamental spaces, were typical in C. marina exposed fish. A surge of plasma lactate occurred in goldlined seabream shortly after exposure to C. marina (0.5h) and sustained throughout the exposure period, indicating rapid onset of and persistent anaerobic respiration in C. marina exposed fish. Depletion of plasma glucose was clearly evident in goldlined seabream showing stress symptoms and near death. Yet, fish alive in the C. marina bloom did not exhibit plasma glucose depletion. The results suggest that availability of fermentable fuel as indicated by glucose level is critical to determine fish survival in C. marina exposure. Overall, our findings have rebuked the involvement of hemolysins and/or nitric oxide as the culprits for C. marina toxicity to fish. This study is the first to demonstrate the pathway of respiratory toxicity induced by the harmful alga C. marina in fish.