Shohag Sheikh, Horie Yoshifumi
Department of Genetic Engineering and Biotechnology, Faculty of Earth and Ocean Science, Bangabandhu Sheikh Mujibur Rahman Maritime University, Dhaka, Bangladesh.
Graduate School of Maritime Science, Kobe University, Kobe, Japan.
J Appl Toxicol. 2025 Mar;45(3):452-459. doi: 10.1002/jat.4718. Epub 2024 Oct 31.
Zinc oxide nanoparticles (ZnO NPs) are widely used in manufacturing cosmetic and pharmaceutical products. Although previous studies have reported their toxic effects on fish, the underlying mechanisms behind their toxic effects are yet to be identified. This study evaluated the impact of ZnO NPs on marine medaka's survival, heart rates (Oryzias melastigma), and the expression of genes linked to neurotoxicity and cardiovascular toxicity. Marine medaka samples were exposed to ZnO NPs at varying concentrations: 0.01, 0.1, 1, and 10 mg/L. Survival rates and heart rates were monitored on the 12th day postfertilization. Gene expression related to neurotoxicity (α-tubulin, elavl3, gap43, gfap) and cardiovascular toxicity (cdh2, atp2a1, cacna1da, crhr1, ahrra, arnt2) was assessed by performing real-time polymerase chain reaction. The survival rate of marine medaka samples was not significantly impacted by exposure to up to 1 mg/L of ZnO NPs; however, exposure to 10 mg/L of ZnO NPs resulted in a 60% reduction in survival rate. The heart rate of the samples did not significantly change across all concentrations. High ZnO NP concentrations (10 mg/L) significantly suppressed the expression of neurotoxic and cardiotoxic genes, including elavl3 and gfap. ZnO NPs exhibited dose-dependent toxic effects on the marine medaka samples by affecting the expression of genes related to neurological and cardiovascular functions. These findings underscore the potential risks of ZnO NPs to aquatic organisms. The distinct toxic actions of ZnO NPs and dissolved ions complicate the interpretation of results, as this study did not measure ion release, a critical factor in understanding NP toxicity. Moreover, ZnO NPs may cause oxidative stress and disrupt cellular pathways. Furthermore, without distinguishing between NP and ion effects, it is challenging to determine the exact cause of toxicity. These findings highlight the need for future studies to measure dissolved ions and particles separately to clarify their contributions to toxicity, where the mechanisms of action are still debated.
氧化锌纳米颗粒(ZnO NPs)广泛应用于化妆品和药品制造。尽管先前的研究报告了它们对鱼类的毒性作用,但其毒性作用背后的潜在机制尚未明确。本研究评估了ZnO NPs对海洋青鳉(Oryzias melastigma)的存活率、心率以及与神经毒性和心血管毒性相关基因表达的影响。将海洋青鳉样本暴露于不同浓度的ZnO NPs:0.01、0.1、1和10 mg/L。在受精后第12天监测存活率和心率。通过实时聚合酶链反应评估与神经毒性(α-微管蛋白、elavl3、gap43、gfap)和心血管毒性(cdh2、atp2a1、cacna1da、crhr1、ahrra、arnt2)相关的基因表达。暴露于高达1 mg/L的ZnO NPs对海洋青鳉样本的存活率没有显著影响;然而,暴露于10 mg/L的ZnO NPs导致存活率降低60%。所有浓度下样本的心率均无显著变化。高浓度的ZnO NPs(10 mg/L)显著抑制了包括elavl3和gfap在内的神经毒性和心脏毒性基因的表达。ZnO NPs通过影响与神经和心血管功能相关的基因表达,对海洋青鳉样本表现出剂量依赖性的毒性作用。这些发现强调了ZnO NPs对水生生物的潜在风险。ZnO NPs和溶解离子的不同毒性作用使结果的解释变得复杂,因为本研究未测量离子释放,而这是理解纳米颗粒毒性的关键因素。此外,ZnO NPs可能会引起氧化应激并扰乱细胞途径。此外,在不区分纳米颗粒和离子作用的情况下,很难确定毒性的确切原因。这些发现凸显了未来研究分别测量溶解离子和颗粒以阐明它们对毒性的贡献的必要性,其作用机制仍存在争议。