Institute of International Rivers and Eco-security, Yunnan Key Laboratory of International Rivers and Trans-Boundary Eco-security, Yunnan University, Kunming, 650091, People's Republic of China; Yunnan International Joint Research Center for Hydro-Ecology Science & Engineering, Yunnan University, Kunming, 650091, People's Republic of China.
Institute of International Rivers and Eco-security, Yunnan Key Laboratory of International Rivers and Trans-Boundary Eco-security, Yunnan University, Kunming, 650091, People's Republic of China.
Environ Pollut. 2020 Jan;256:113504. doi: 10.1016/j.envpol.2019.113504. Epub 2019 Oct 31.
Although the toxicity of silver nanoparticles (AgNPs) in aquatic organisms has been extensively investigated, the mechanism by which AgNPs damage membranes remains unclear. This study investigated the toxic effects of a series of sub-lethal concentrations of AgNPs on the membranes of freshwater carp (Cyprinus carpio) gills, based on changes in membrane fatty acid (FA) profile, membrane fluidity, membrane lipid peroxidation, and histopathology. Most of the FAs in fish gill membrane was not significantly affected by exposure to multiple AgNPs concentrations, only few significant changes occurred in some specific FAs species at a high concentration of AgNPs exposure. In particular, high concentrations of AgNPs significantly decreased the proportions of two important long-chain n-3 series polyunsaturated FAs (C20: 5n3, and C22: 6n3), resulting in a decreased ratio of n-3 polyunsaturated FAs to n-6 polyunsaturated FAs (Σn-3UFA/Σn-6UFA). The AgNPs also caused a dose-dependent decrease in fish gill membrane fluidity, increased the level of lipid peroxidation, and inhibited Na/K-ATPase enzyme activity. Further histopathological examination revealed that exposure to AgNPs can cause toxic responses in the lamellae, including the thinning of the basement membrane, malformation, and inflammation. Together, the results suggest that the mechanism of AgNPs membrane toxicity involves the oxidization of long-chain omega-3 unsaturated FAs to saturated FAs via lipid peroxidation, resulting in, decreased membrane fluidity and ultimately the destruction of the normal physiological function of the fish gill membrane. The findings contribute significantly to our understanding of nanoparticle-induced membrane toxicity and potential risks in aquatic environments.
虽然银纳米粒子（AgNPs）在水生生物中的毒性已经得到了广泛的研究，但 AgNPs 破坏膜的机制仍不清楚。本研究基于膜脂肪酸（FA）谱、膜流动性、膜脂质过氧化和组织病理学的变化，研究了一系列亚致死浓度的 AgNPs 对淡水鲤鱼（Cyprinus carpio）鳃膜的毒性作用。暴露于多种 AgNPs 浓度下，鱼鳃膜中的大多数 FA 没有显著变化，只有在高浓度 AgNPs 暴露下，一些特定的 FA 种类发生了一些显著变化。特别是，高浓度的 AgNPs 显著降低了两种重要的长链 n-3 系列多不饱和 FA（C20:5n3 和 C22:6n3）的比例，导致 n-3 多不饱和 FA 与 n-6 多不饱和 FA 的比例降低（Σn-3UFA/Σn-6UFA）。AgNPs 还导致鱼鳃膜流动性呈剂量依赖性下降，脂质过氧化水平升高，并抑制 Na/K-ATPase 酶活性。进一步的组织病理学检查显示，AgNPs 暴露会引起鳃片的毒性反应，包括基底膜变薄、畸形和炎症。总之，研究结果表明，AgNPs 膜毒性的机制涉及通过脂质过氧化将长链ω-3 不饱和 FA 氧化为饱和 FA，导致膜流动性降低，最终破坏鱼鳃膜的正常生理功能。这些发现对我们理解纳米颗粒诱导的膜毒性和水生环境中的潜在风险具有重要意义。
