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Title: Cytological and physiological responses in goldlined seabream (rhabdosargus sarba) upon exposure to the harmful algal species chattonella marina
Other Titles: Chi chao hai yang he bao zao dui jin si yu zhi bing li sheng li xue
Authors: Tang, Janet Yat Man (鄧逸敏)
Department: Dept. of Biology and Chemistry
Degree: Doctor of Philosophy
Issue Date: 2005
Publisher: City University of Hong Kong
Subjects: Algal blooms
Rhabdosargus sarba
Toxic marine algae
Notes: CityU Call Number: QK568.T67 T36 2005
Includes bibliographical references (leaves 107-124)
Thesis (Ph.D.)--City University of Hong Kong, 2005
xxii, 125 leaves : ill. (some col.) ; 30 cm.
Type: Thesis
Abstract: Harmful algal blooms (HABs) have increased in frequency, intensity and geographic distribution over the past few decades. The ichthyotoxic raphidophyte Chattonella marina has caused severe economic losses in mariculture industry all over the world. The toxic mechanism caused on fish by this notorious HAB causative species remains unresolved. Severe gill pathological damage has been reported when fish were exposed to bloom concentrations of C. marina. Surprisingly, no studies have been conducted to relate gill pathology to associated functional impairments of the fish. Such information will be very useful to explain the physiological effects of toxic C. marina on marine fish and, thereby the cause of fish death. On the other hand, the ability of C. marina to produce reactive oxygen species (ROS), in cultures has led to various speculations that ROS is the putative agent responsible for these fish kills. To date, there is inadequate evidence to relate ROS concentrations produced by C. marina with gill damage and eventual fish death. Furthermore, low concentrations of Chattonella are commonly found in coastal waters. Previous toxicity studies of C. marina have been solely based upon acute exposure of fish to bloom concentrations of the toxic alga. It remains unknown whether exposure to sub-bloom concentrations of C. marina cause similar adverse physiological and pathological effects in marine fish. We here hypothesize that ROS produced by sub-bloom and bloom concentrations of C. marina cause gill damage, which leads to physiological impairments, chronic pathological responses, and eventual fish death. The goldlined seabream Rhabdosargus sarba, a local mariculture fish, was chosen for the present study. The objectives of this thesis are (1) to investigate gill cytopathology and associate changes in blood partial oxygen concentration (pO2) and osmolality in fish exposed to sub-bloom and bloom levels of C. marina; (2) to compare physiological and pathological changes in fish exposed to C. marina and ROS, with the aim of identifying the role of ROS in fish mortality. Based on the first part of the experimental results, abrupt salinity stress experiments and immunocytological study of osmoregulatory protein transporters in chloride cells were conducted to determine whether the observed ichthyotoxicity of C. marina was mediated through osmoregulatory failure of filamental chloride cells (CCs) of fish gill. The mean lethal time (LT50 ) upon exposure of goldlined seabream to bloom (8000 cells/ml) and sub-bloom concentrations (2000 cells/ml) of C. marina was 1 h and 3 h, respectively. Significant induction of filamental CCs (i.e. increases in CC density, apical opening area, fractional area, volume densities of CCs and mitochondria within CCs), coupled with a significant reduction in blood osmolality, was found in fish exposed to C. marina. Reduced blood osmolality (ca. 60%), along with a drastic decline of blood pOz (ca. 15 - 70%), was found in all moribund fish. Evidently, C. marina, even in concentrations below visible blooms, can pose a significant threat to marine fish. Similar physiological and cytopathological changes, however, were not observed in fish exposed to the most prevalent species of ROS [hydrogen peroxide (H202)] at both 0.5 mM and 1.0 mM concentrations (equivalent to 25x and 50x of the amount produced by C. marina). Non-specific damage of gill membranes (i.e. severe loss of microvilli projections on CC apical opening and rupture of epithelial membrane in the lamellae) was evident in the H202 treatments only, and this type of gill damage was not observed in fish exposed to C. marina. Moribund fish in the H202 treatments showed no sign of osmotic distress. Our physiological and cytological evidence suggests that ROS is not the principal toxic agent in fish mortalities from C. marina exposure. In the salinity stress experiments, fish were abruptly transferred to hyper- (O%o) and hypo-(60%o) salinities. Our quantitative ultrastructural and physiological data showed that fish exposed to sub-bloom concentration of C. marina suffered similar but more severe osmotic distress than that induced by abrupt transfer to 6O%0 hypersaline water. Results also showed that suffocation was not a secondary response induced by osmotic impairment in the moribund fish. Our quantitative immunocytological study demonstrated for the first time that the key osmoregulatory proteins, Na+, K+ -ATPase cystic fibrosis transmembrane regulator (CFTR)-like Cl- channel, on gill CCs were induced (ca. 50%) upon exposure to sub-bloom concentration of C. marina (2000 cells/ml). These results indicate that hyperactive excretion of Na+ and C1- from gill CCs is the most likely cause of blood osmolality declines. Osmoregulatory failure in conjunction with suffocation may be the principal cause of fish mortalities following exposure to C. marina.
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