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 Ca²⁺, 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.

有害的藻华（HAB）是造成g鱼明显损坏而造成野生鱼类和水产养殖鱼类大量死亡的原因，但确切的杀鱼机制仍知之甚少。非侵入性微电极离子通量估计（MIFE）技术已成功应用于评估暴露于有害微浮游生物的模型鱼g细胞系中膜转运过程的变化。在加入该麻痹性贝类毒素（PST）生产者的裂解细胞以及纯化的胞内鞭毛鞭毛虫PST之前和之后，监测虹鳟细胞系RTgill-W1中的净Ca 2 ⁺，H ⁺，K ⁺离子通量。已证明，仅PST不会在A. catenella期间对鱼ill造成损害如先前所认为的那样爆发，但是来自裂解藻类细胞的其他鱼腥毒素代谢产物（即脂质过氧化产物或其他未知代谢产物）导致鱼g细胞的净K ⁺外排，从而导致g细胞死亡。