The current study is based on the increasing demand for the assessment of ionic liquid (IL)-mediated aquatic toxicity. Specifically, although a lot of studies have been performed so far, investigating IL-mediated adverse effects on numerous aquatic organisms, little is known about their mode of action. Given that the use of in vitro models is considered as a reliable tool for determining the mediated biological effects, the modulation of specific biochemical pathways and the onset of various forms of damage with great precision and reproducibility, mixed primary cultures of mussel Mytilus galloprovincialis hemocytes were used for investigating whether 1-octyl-3-methylimidazolium tetrafluoroborate ([omim][BF₄]) mediated toxicity is related to its interaction with cellular membrane proteins. Specifically, [omim][BF₄]-mediated cytotoxic, oxidative and genotoxic effects were investigated in mussel hemocytes before and after pre-treatment of cells with non-toxic concentration of guanidine hydrochloride (1 mM GndHCl). The results showed that [omim][BF₄] at concentrations ranging from 0.7 to 1.75 μM can induce cytotoxic (almost <50% reduction of cell viability), oxidative (increased levels of O₂^•− production and lipid peroxidation by-products) and genotoxic (increased levels of DNA damage) effects, while cells pre-treated with 1 mM GndHCl showed a significant attenuation of IL’s toxic potency in all cases. According to the latter, the current study showed that [omim][BF₄]-mediated toxicity could be related not only to its well-known interaction with membrane lipid bilayers, but also to its interference with membrane proteins. Using GndHCl, a chaotropic agent that disrupts the hydrogen bonding network and the stability of membrane proteins via its interference with the intramolecular interactions mediated by non-covalent forces on cellular membranes, it was firstly shown that altering the membrane integrity as well as the native state of cellular membrane proteins, by weakening the hydrophobic effect, could attenuate the possible interaction of [omim][BF₄] with cellular membranes and the concomitant induction of protein-based intracellular processes, commonly linked with the induction of severe cellular damage.

当前的研究是基于对评估离子液体（IL）介导的水生毒性的日益增长的需求。具体而言，尽管到目前为止已进行了大量研究，以调查IL介导的对多种水生生物的不良影响，但对其作用方式知之甚少。考虑到使用体外模型被认为是确定介导的生物学效应，特定生化途径的调节以及各种形式的损害的发作具有很高的精度和可重复性的可靠工具，贻贝Mytilus galloprovincialis血细胞的混合原代培养是用于研究四氟硼酸1-辛基-3-甲基咪唑鎓（[omim] [BF ₄]）介导的毒性与其与细胞膜蛋白的相互作用有关。具体地，在用无毒浓度的盐酸胍（1 mM GndHCl）预处理细胞之前和之后，研究贻贝血细胞中[omim] [BF ₄ ]介导的细胞毒性，氧化和遗传毒性作用。结果表明，[omim] [BF ₄ ]的浓度在0.7到1.75μM之间，可诱导细胞毒性（几乎降低了50％的细胞活力），氧化作用（O ₂ ^•-水平升高）生产和脂质过氧化副产物）和遗传毒性（DNA损伤水平增加）的影响，而用1 mM GndHCl预处理的细胞在所有情况下均显着减弱了IL的毒性。根据后者，目前的研究表明[omim] [BF ₄介导的毒性不仅与其与膜脂质双层的众所周知的相互作用有关，而且与其对膜蛋白的干扰有关。使用GndHCl，一种离液剂，通过干扰细胞膜上非共价力介导的分子内相互作用，破坏氢键网络和膜蛋白的稳定性，首先证明了改变膜完整性和天然状态细胞膜蛋白的合成，通过减弱疏水作用，可以减弱[omim] [BF ₄ ]与细胞膜的可能相互作用以及伴随蛋白质的细胞内过程的诱导，通常与诱导严重的细胞损伤有关。