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Title: Unraveling the fish kill mechanism(s) of the harmful alga Chattonella marina, from the perspective of osmotic disturbance
Other Titles: You hai hai yang he bao zao de yu du xing : dui yu lei shen tou ya tiao jie de gan rao
有害海洋褐胞藻的魚毒性 : 對魚類滲透壓調節的干擾
Authors: Xu, Jingliang (徐景亮)
Department: Department of Biology and Chemistry
Degree: Doctor of Philosophy
Issue Date: 2010
Publisher: City University of Hong Kong
Subjects: Chrysophyceae -- Toxicology.
Toxic marine algae -- Toxicology.
Fishes -- Effect of water pollution on.
Notes: CityU Call Number: QK569.C62 X8 2010
xvii, 125 leaves : ill. (some col.) 30 cm.
Thesis (Ph.D.)--City University of Hong Kong, 2010.
Includes bibliographical references (leaves 105-125)
Type: thesis
Abstract: The harmful algal bloom (HAB) species, Chattonella marina, has caused severe economic loss to marine fisheries worldwide. In the past three decades, suffocation or respiratory disorder has been seen as the major mechanism responsible for fish kills from C. marina. However, recent studies have shown that osmotic distress is another probable cause of death of fish exposed to the toxic C. marina. Changes in gill chloride cells (both in density and number) and blood osmolality have been reported in goldlined seabream (Rhabdosargus sarba) exposed to C. marina. However, the precise toxic mechanism(s), i.e. precisely how C. marina induces such physiological impairments in marine fish is virtually unknown. Consequently the generally accepted reason(s) for the fish deaths must be seen as highly controversial. The present study attempted to identify the fish kill mechanisms linked to this toxic HAB species. We hypothesized that the effects of C. marina on fish are due to a disruption of osmotic homeostasis. More specifically, we proposed that plasma osmolality would increase following exposure to C. marina via one or more of the following pathways: i) inhibition of NaCl secretion in fish gill; ii) disruption to paracellular tight junction of fish gill and gastrointestinal (GI) tract epithelium, and/or iii) inhibition of the water uptake process at the GI tract. By comparing fish susceptibility to C. marina using fish species with different osmoregulatory and respiratory capacities, we would be able to identify the major cause of fish kills by C. marina. Three local marine fish species, goldlined seabream (Rhabdosargus sarba), Russell's snapper (Lutjanus russellii), and green grouper (Epinephelus coioides) were chosen for the fish susceptibility study. The osmoregulatory and respiratory capacities of these species were compared by subjecting the fish to acute hypertonic seawater and hypoxia exposure. Based on the mortality results (LT50), the order of hypoxia tolerance was identified as: green grouper > Russell's snapper > goldlined seabream; while the hypertonic seawater tolerance was comparable in all three species with similar LT50 around 3 h. When the three fish species were exposed to bloom concentration of C. marina (10,000 cells/ml), the goldlined seabream was found to be most susceptible to C. marina (LT50 = 5.1 h), followed by the Russell's snapper (LT50 = 7.5 h). Fish that died as a result of C. marina exposure all exhibited a significant elevation of plasma osmolality. However, the relationship between blood partial pressure of oxygen (pO2) and fish mortality was not consistent. For example, significant decline of pO2 was found in C. marina stressed goldlined seabream, but not in C. marina stressed Russell's snapper. The green grouper was most tolerant to C. marina. No fish mortality or osmotic disruption was observed in this species throughout the exposure period (48 h), despite the fact that the blood pO2 decreased by up to 68%. These findings suggest that disturbance of osmotic balance is an important mechanism involved in fish kills by C. marina, and that this disruption is independent of decreases in pO2. No significant change was observed in gill Na+-K+-ATPase (NKA) activity in goldlined seabream following exposure to C. marina. Therefore, inhibition of NaCl secretion from gills is unlikely to be the cause of abnormal elevation of Na+, Cl- levels in the plasma of fish exposed to C. marina. In the green grouper, a C. marina tolerant species, the levels of gill cyclic adenosine monophosphate (cAMP, a major component of osmoregulatory signal transduction) and plasma cortisol (a crucial osmoregulatory hormone) increased 5.4 and 1.3-fold respectively within 1 h of exposure to C. marina, and returned to the control levels after 6 h. Activation of these energetic regulatory processes could stimulate rapid NaCl secretion from the gills, which may be a response by the green grouper to the osmotic stress induced by C. marina. The green groupers also secreted copious amount of mucus which covered their gills and which may prevent direct contact with the toxic C. marina. To further investigate whether C. marina could directly affect the integrity of paracellular tight junction (TJ) in fish epithelia, the esophageal epithelium of goldlined seabream was isolated and mounted onto an Ussing system. The tissue was subsequently exposed to C. marina and changes in transepithelial resistance (TER) were recorded. The TER data confirm that the paracellular tight junction on the esophageal epithelium could be loosened by direct exposure to C. marina. Two modes of action for C. marina on TJ integrity were discovered - one is fast-acting and reversible (C. marina cells at the exponential growth phase), while the other is accumulative and irreversible (C. marina cells at the stationary growth phase). Loosening of paracellular TJs between fish blood and hypertonic external seawater will undoubtedly accelerate the entry of seawater ions into fish blood and at the same time promote loss of water content from blood into seawater. As a result, the plasma osmolality in fish will increase rapidly and significantly. In addition, we found a concomitant increase of gut fluid osmolality in goldlined seabream during C. marina exposure, suggesting the desalination process could be inhibited, and insufficient H2O absorption from the gut might be an additional cause of elevation of plasma osmolality. Overall, findings of the present study provide a major breakthrough on understanding of the fish kill mechanisms linked to the harmful algal species, C. marina. Strong links between fish death and increased osmolality have been observed. Metabolic processes involved in NaCl secretion from the gills may be a mechanism for dealing with osmotic stress following exposure to C. marina. NaCl secretion from the gills is unlikely to be the cause of this increased plasma osmolality. Importantly, this study provides new evidence that elevation of plasma ions and osmolality in fish exposed to C. marina is mediated directly via a disruption of epithelial paracellular tight junction. Further studies on the direct effects of isolated C. marina toxins on major TJ core components are therefore suggested.
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