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Ichthyotoxicity of a Harmful Dinoflagellate Cochlodinium polykrikoides: Aspect of Hematological Responses of Fish Exposed to Algal Blooms
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  • Ichthyotoxicity of a Harmful Dinoflagellate Cochlodinium polykrikoides: Aspect of Hematological Responses of Fish Exposed to Algal Blooms
  • Ichthyotoxicity of a Harmful Dinoflagellate Cochlodinium polykrikoides: Aspect of Hematological Responses of Fish Exposed to Algal Blooms
저자명
Kim. Chang Sook,Bae. Heon Meen,Yun. Seong Jong,Cho. Yong Chul,Kim. Hak Gyoon
간행물명
Journal of fisheries science and technology
권/호정보
2000년|3권 2호|pp.111-117 (7 pages)
발행정보
한국수산학회
파일정보
정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

To clarify the ichthyotoxic mechanisms of a harmful dinoflagellate Cochlodinium polykrikoides, hematological responses of the flounder Paralichthys olivaceus and red sea bream Pagrus major exposed to this algal bloom were investigated. The mortality of red sea bream was considerably larger than that of flounder, and the threshold lethal density of C. polykrikoides to the test fish was approximately 3,000 cells/ml. Blood $PO_2$declined in proportion to the increasing density of algal cells. The blood $PO_2$ of moribund fish was about $40-60\% of control test fish. Particularly, the fishes began to be killed when the blood $PO_2$ fell below 30-40 mmHg. However, the blood pH dropped almost 1.0 unit just before fish kill. Hemoglobin and hematocrit levels of fish exposed to C. polykrikoides of 5,000 cells/ml for 24 h and of moribund fish did not show great difference. The concentrations of plasma $Na^+$, $K^+$ and $Cl^-$ were slightly elevated to different magnitudes except $Ca^{2+}$ and plasma osmolality was also increased in Cochlodinium-exposed fish. In the plasma cortisol level, these values of moribund flounder and red sea bream were 4- 5 times higher than those of control fish. These results suggest that the drop of blood $PO_2$ was may be one of the principal causes of fish kill by C. polykrikoides, and the changes of other hematological parameters were secondary responses elicited by the decrease in blood $PO_2$.