Neurotoxicity and Cardiovascular Toxicity of Zinc Oxide Nanoparticles to Oryzias melastigma.

IF 2.7 4区 医学 Q3 TOXICOLOGY
Sheikh Shohag, Yoshifumi Horie
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引用次数: 0

Abstract

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.

氧化锌纳米颗粒对黑鲔鱼的神经毒性和心血管毒性
氧化锌纳米粒子(ZnO NPs)被广泛用于制造化妆品和医药产品。尽管之前的研究已经报道了其对鱼类的毒性作用,但其毒性作用背后的潜在机制仍有待确定。本研究评估了氧化锌氮氧化物对水鳉(Oryzias melastigma)的存活率、心率以及与神经毒性和心血管毒性相关的基因表达的影响。青鳉样本暴露于不同浓度的氧化锌氮氧化物:0.01、0.1、1 和 10 毫克/升。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了与神经毒性(α-tubulin、elavl3、gap43、gfap)和心血管毒性(cdh2、atp2a1、cacna1da、chrr1、ahrra、arnt2)相关的基因表达。暴露于最多 1 毫克/升的氧化锌氮氧化物时,青鳉样本的存活率没有受到明显影响;但暴露于 10 毫克/升的氧化锌氮氧化物时,存活率降低了 60%。样本的心率在所有浓度下均无明显变化。高浓度 ZnO NP(10 毫克/升)明显抑制了神经毒性基因和心脏毒性基因的表达,包括 elavl3 和 gfap。氧化锌氮氧化物通过影响神经和心血管功能相关基因的表达,对水鳉样本产生了剂量依赖性毒性效应。这些发现强调了氧化锌氮氧化物对水生生物的潜在风险。氧化锌氮氧化物和溶解离子的不同毒性作用使结果的解释变得复杂,因为这项研究没有测量离子释放量,而离子释放量是了解氮氧化物毒性的关键因素。此外,氧化锌氮氧化物可能会导致氧化应激,破坏细胞通路。此外,如果不区分氮氧化物和离子的影响,就很难确定毒性的确切原因。这些发现突出表明,今后的研究需要分别测量溶解的离子和微粒,以明确它们对毒性的影响,而对其作用机制仍存在争议。
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来源期刊
CiteScore
7.00
自引率
6.10%
发文量
145
审稿时长
1 months
期刊介绍: Journal of Applied Toxicology publishes peer-reviewed original reviews and hypothesis-driven research articles on mechanistic, fundamental and applied research relating to the toxicity of drugs and chemicals at the molecular, cellular, tissue, target organ and whole body level in vivo (by all relevant routes of exposure) and in vitro / ex vivo. All aspects of toxicology are covered (including but not limited to nanotoxicology, genomics and proteomics, teratogenesis, carcinogenesis, mutagenesis, reproductive and endocrine toxicology, toxicopathology, target organ toxicity, systems toxicity (eg immunotoxicity), neurobehavioral toxicology, mechanistic studies, biochemical and molecular toxicology, novel biomarkers, pharmacokinetics/PBPK, risk assessment and environmental health studies) and emphasis is given to papers of clear application to human health, and/or advance mechanistic understanding and/or provide significant contributions and impact to their field.
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