有害甲藻米氏凯伦藻（Karenia mikimotoi）对海洋青鳉鱼（Oryzias melastigm）的急性毒性效应研究

米氏凯伦藻（Karenia mikimotoi）是我国近岸海域常见的有毒有害藻华肇事种，能产生多种毒素，其发生藻华时会使大量鱼类或贝类死亡。本研究从细胞生物学、氧化和免疫酶活性角度研究米氏凯伦藻对海洋青鳉鱼（Oryzias melastigma）的急性毒性效应（72 h），以期揭示米氏凯伦藻对鱼类的致死原因。组织切片结果表明，高浓度的米氏凯伦藻（1.37～1.52）×107 cells/L]可以导致海洋青鳉鱼鳃丝断裂，成团状与相邻鳃丝融合，鳃丝上皮细胞的细胞核发生偏移，并使肝细胞出现空泡化现象。高浓度的米氏凯伦藻能够抑制海洋青鳉鱼的鳃和肝组织的SOD酶活性和CAT酶活性，引起海洋青鳉鱼脂质过氧化，导致丙二醛（MDA）含量升高，对组织造成损伤。本研究结果表明，米氏凯伦藻可能通过氧化应激反应使海洋青鳉鱼的鳃和肝组织受损，为深入阐明米氏凯伦藻的毒性机制提供参考。

Study on the acute toxicity effects of harmful dinoflagellate Karenia mikimotoi to Oryzias melastigm

Karenia mikimotoi, a frequently toxic and harmful bloom-forming species in China's coastal waters, could produce multi-toxins and cause considerable death of fishes or shellfishes when it blooms. The acute toxicity effects (72 h) of K. mikimotoi to fish Oryzias melastigma from cell biology, cell oxidation and immune enzyme activities have been studied and hence to find out how K. mikimotoi killed the fishes. Exposing to a high concentration of K. mikimotoi (1.37～1.52)×107 cells/L], results of tissue sections in O. melastigma showed that gill filaments were broken and merged with nearby filaments as lumpy forms, positions shifting of epithelial cell nucleus for gills, and vacuolation occurred in liver cells. The high concentration of K. mikimotoi inhibited enzyme activities of superoxide dismutase (SOD) and catalase (CAT) in gill and liver cells and increased contents of malondialdehyde (MDA) for O. melastigma. It caused over-oxidation of cell membrane lipid and damage to tissue structure. Our results suggested that K. mikimotoi caused damage to gill and liver cellsof O. melastigma via oxidative stress, which provides an insight into the toxicity mechanism of K. mikimotoi.