TY - JOUR
T1 - Hydrogen peroxide is not the cause of fish kills associated with Chattonella marina
T2 - Cytological and physiological evidence
AU - Tang, Janet Y. M.
AU - Anderson, Donald M.
AU - Au, Doris W. T.
PY - 2005/5/15
Y1 - 2005/5/15
N2 - Chattonella marina, a harmful algal bloom (HAB) causative species, was used to study the mortality, physiology, and pathology of a marine stenohaline fish, goldlined seabream exposed to the toxic alga. The median lethal time (LT 50) was 3 h upon exposure to 8000 cells/ml of C. marina. Significant induction of filamental chloride cells (CCs) [i.e. increases in CC fractional area and in the volume density of CCs], concomitant with significant reduction of blood osmolality, were found in C. marina treated fish. To verify whether the toxicity of C. marina was mediated through oxidative stress, a hydrogen peroxide exposure experiment was carried out and the toxicity as well as cytological and physiological changes were compared with the C. marina treatment. Hydrogen peroxide at a concentration of 500 μM H2O 2, (i.e. 25 times higher than that produced by 8000 cells/ml of C. marina (20 μM H2O2)) was unable to induce similar CC alterations and osmoregulatory impairment in fish as observed in the C. marina treatment. Non-specific membrane damage such as severe loss of microvilli projections on the CC apical opening and rupture of epithelial membranes in the lamellae were observed. The LT50 was 6 h, two times longer than that with 8000 cells/ml of C. marina. Based on the cytological and physiological evidence and toxicity data, the mechanism by which C. marina kills fish appears to be very different from that caused by H2O2/ROS. Osmoregulatory distress is the major cause of fish death upon exposure to C. marina. © 2005 Elsevier B.V. All rights reserved.
AB - Chattonella marina, a harmful algal bloom (HAB) causative species, was used to study the mortality, physiology, and pathology of a marine stenohaline fish, goldlined seabream exposed to the toxic alga. The median lethal time (LT 50) was 3 h upon exposure to 8000 cells/ml of C. marina. Significant induction of filamental chloride cells (CCs) [i.e. increases in CC fractional area and in the volume density of CCs], concomitant with significant reduction of blood osmolality, were found in C. marina treated fish. To verify whether the toxicity of C. marina was mediated through oxidative stress, a hydrogen peroxide exposure experiment was carried out and the toxicity as well as cytological and physiological changes were compared with the C. marina treatment. Hydrogen peroxide at a concentration of 500 μM H2O 2, (i.e. 25 times higher than that produced by 8000 cells/ml of C. marina (20 μM H2O2)) was unable to induce similar CC alterations and osmoregulatory impairment in fish as observed in the C. marina treatment. Non-specific membrane damage such as severe loss of microvilli projections on the CC apical opening and rupture of epithelial membranes in the lamellae were observed. The LT50 was 6 h, two times longer than that with 8000 cells/ml of C. marina. Based on the cytological and physiological evidence and toxicity data, the mechanism by which C. marina kills fish appears to be very different from that caused by H2O2/ROS. Osmoregulatory distress is the major cause of fish death upon exposure to C. marina. © 2005 Elsevier B.V. All rights reserved.
KW - Chattonella marina
KW - Fish kill mechanism
KW - HAB
KW - Harmful algal bloom
KW - Osmoregulation
KW - Quantitative ultrastructure
KW - Reactive oxygen species
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UR - https://www.scopus.com/record/pubmetrics.uri?eid=2-s2.0-17444415306&origin=recordpage
U2 - 10.1016/j.aquatox.2005.01.007
DO - 10.1016/j.aquatox.2005.01.007
M3 - RGC 21 - Publication in refereed journal
C2 - 15848254
SN - 0166-445X
VL - 72
SP - 351
EP - 360
JO - Aquatic Toxicology
JF - Aquatic Toxicology
IS - 4
ER -