Mechanisms of nanoparticle-induced oxidative stress and toxicity.

Mechanisms of nanoparticle-induced oxidative stress and toxicity.
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DOI:
10.1155/2013/942916
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发表时间:
2013
影响因子:
--
通讯作者:
Rojanasakul Y
Rojanasakul Y
中科院分区:
生物学3区
文献类型:
--
作者:
Manke A;Wang L;Rojanasakul Y

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迅速崛起的纳米技术领域为医疗、工业和消费领域提供了创新发现。工程纳米粒子(NP)独特的物理化学和电学性质使其在各种应用中非常受欢迎。然而,NP的这些新特性充满了对环境和职业暴露的担忧。NP的结构和物理化学性质的变化可导致生物活性的变化,包括ROS的产生,这是最常报道的NP相关毒性之一。由工程化NP诱导的氧化应激是由于非细胞因素如颗粒表面、大小、组成和金属的存在,而细胞反应如线粒体呼吸、NP-细胞相互作用和免疫细胞活化是ROS介导的损伤的原因。NP诱导的氧化应激反应是进一步病理生理学效应的火炬传递者,包括遗传毒性、炎症和纤维化,如通过激活相关细胞信号传导途径所证明的。由于氧化应激是NP诱导损伤的关键决定因素,因此有必要表征NP引起的ROS反应。通过物理化学表征和理解的多个信号级联激活的NP诱导的ROS,全身毒性筛选与氧化应激作为NP诱导的损伤的预测模型可以开发。
The rapidly emerging field of nanotechnology has offered innovative discoveries in the medical, industrial, and consumer sectors. The unique physicochemical and electrical properties of engineered nanoparticles (NP) make them highly desirable in a variety of applications. However, these novel properties of NP are fraught with concerns for environmental and occupational exposure. Changes in structural and physicochemical properties of NP can lead to changes in biological activities including ROS generation, one of the most frequently reported NP-associated toxicities. Oxidative stress induced by engineered NP is due to acellular factors such as particle surface, size, composition, and presence of metals, while cellular responses such as mitochondrial respiration, NP-cell interaction, and immune cell activation are responsible for ROS-mediated damage. NP-induced oxidative stress responses are torch bearers for further pathophysiological effects including genotoxicity, inflammation, and fibrosis as demonstrated by activation of associated cell signaling pathways. Since oxidative stress is a key determinant of NP-induced injury, it is necessary to characterize the ROS response resulting from NP. Through physicochemical characterization and understanding of the multiple signaling cascades activated by NP-induced ROS, a systemic toxicity screen with oxidative stress as a predictive model for NP-induced injury can be developed.
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