Institute for Marine and Antarctic Studies (IMAS), University of Tasmania, Private Bag 129, Hobart, Tasmania 7001, Australia; Centro de Estudios de Algas Nocivas (CREAN), Instituto de Fomento Pesquero (IFOP), Puerto Montt, Chile.
School of Land and Food, University of Tasmania, Private Bag 54, Hobart, Tasmania 7001, Australia.
Harmful Algae. 2018 Dec;80:55-63. doi: 10.1016/j.hal.2018.09.004. Epub 2018 Sep 28.
Harmful algal blooms (HAB) are responsible for massive mortalities of wild and aquacultured fish due to noticeable gill damage, but the precise fish-killing mechanisms remain poorly understood. A non-invasive microelectrode ion flux estimation (MIFE) technique was successfully applied to assess changes in membrane-transport processes in a model fish gill cell line exposed to harmful microplankton. Net Ca, H, K ion fluxes in the rainbow trout cell line RTgill-W1 were monitored before and after addition of lysed cells of this Paralytic Shellfish Toxins (PST) producer along with purified endocellular dinoflagellate PST. It was demonstrated that PST alone do not play a role in fish gill damage during A. catenella outbreaks as previously thought, but that other ichthyotoxic metabolites from lysed algal cells (i.e. lipid peroxidation products or other unknown metabolites) result in net K efflux from fish gill cells and thereby gill cell death.
有害藻华(HAB)会导致大量野生和水产养殖鱼类死亡,这主要是由于鱼类的鳃严重受损,但鱼类致死的确切机制仍不清楚。非侵入性微电极离子通量估计(MIFE)技术成功地应用于评估暴露于有害微浮游生物的鱼类鳃细胞系中膜转运过程的变化。在添加麻痹性贝类毒素(PST)生产者的裂解细胞以及纯化的内共生甲藻 PST 之前和之后,监测虹鳟鱼细胞系 RTgill-W1 的净 Ca、H、K 离子通量。结果表明,PST 本身在以前认为的鱼腥藻爆发期间并没有在鱼类鳃损伤中起作用,而是来自裂解藻类细胞的其他鱼毒性代谢物(即脂质过氧化产物或其他未知代谢物)导致鱼类鳃细胞的净 K 外流,从而导致鳃细胞死亡。