摘要
近年来,米氏凯伦藻(Karenia mikimotoi)已成为我国海域主要的有毒赤潮藻。仅2012年在我国浙江和福建海域就连续爆发了12起米氏凯伦藻赤潮,造成大量养殖鲍死亡,经济损失超过20亿元人民币。本研究通过收集国内外最新报道,探讨了米氏凯伦藻赤潮对各类海洋生物,主要包括海洋浮游动物、贝类、鱼类以及哺乳类毒性作用的研究进展。研究发现,溶血毒素是米氏凯伦藻赤潮引发海洋生物大量死亡的主要原因;直接接触活的米氏凯伦藻细胞是导致浮游动物死亡的主要途径;米氏凯伦藻产生的溶血毒素和鱼毒素,可溶解鱼类的鳃组织,从而造成鱼类死亡。然而,关于米氏凯伦藻产生的溶血毒素是否会在贝类体内累积、在贝类体内的迁移和转化规律、米氏凯伦藻赤潮对鲍鱼死亡的致死途径与致死机制、溶血毒素在生物链传递过程中是否会发生改变、这些毒素对人类健康的影响机制与综合作用等问题还不了解,亟待深入的研究。米氏凯伦藻溶血毒素的研究报道还处于起步阶段,毒素以何种方式导致红细胞破裂,不同红细胞膜上组份的差异和毒素的溶血活性是否存在对应关系等,这些问题都需要我们开展进一步的研究。
Red tide Causing by Karenia mikimotoi has become the main toxic algae bloom in China sea in recent years.For example,12 red tide events caused by Karenia mikimotoi continuously happened in Chinese Zhejiang and Fujian provinces in 2012,resulting in a mass death of aquaculture animals,making economic loss of more than 2 billion Yuan.Toxic effects of Karenia mikimotoi on various types of marine organisms including of marine zooplankton,shellfish,fish and mammalian were discussed here based on summarizing domestic and foreign latest research progresses.The results showed that hemolytic toxin from Karenia mikimotoi was the main reason causing death of marine organisms.Directly contacting with live Karenia mikimotoi was the main way leading to zooplankton death;Karenia mikimotoi can produce hemolytic toxin and ichthyotoxin,which could lysis gill tissue of fish,then caused the fish death.However,the accumulation,migration and transformation law of Karenia mikimotoi hemolytic toxin in shellfish,the lethal way and the mechanism of Karenia mikimotoi causing abalone death,whether the hemolytic toxin change when transferring in the food chain and whether the toxins can damage human health and so on are not clear and need further research.Researchs about Karenia mikimotoi hemolytic toxin are still in the primary stage,questions like how toxin lead to red blood cells rupture,whether hemolytic toxin in the red cell membrane has specific binding sites,is there any corresponding relationship between hemolytic activity and erythrocyte membrane,should be further explored.
引文