The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles.
By Ning Li, Tian Xia, A. Nel. Free Radical Biology & Medicine, 2008
906 citations recorded by the source corpus.
Subfields: Health, Toxicology and Mutagenesis, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/3936a2fe911fc0e6891827db68e04680690fd075
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In Health, Toxicology and Mutagenesis
Citations in the corpus
- Size-dependent cytotoxicity of silver nanoparticles in human lung cells: the role of cellular uptake, agglomeration and Ag release (2014, background): “damage may potentially be explained by ROS generation [32].”
- A review on biosynthesis of silver nanoparticles and their biocidal properties (2018, background): “Very recently [269], it has been investigated that Ag NPs in conjugation with other metals such as TiO2@Ag nanoparticles act against leishmaniasis.”
- Pulmonary Oxidative Stress, Inflammation and Cancer: Respirable Particulate Matter, Fibrous Dusts and Ozone as Major Causes of Lung Carcinogenesis through Reactive Oxygen Species Mechanisms (2013, neutral): “(enzyme) oxidative damage [57–59].”
- Mechanisms of Nanoparticle-Induced Oxidative Stress and Toxicity (2013, background): “Most work to date has suggested that ROS generation (which can be either protective or harmful during biological interactions) and consequent oxidative stress are frequently observed with NP toxicity [3, 9].”
- Autophagy and lysosomal dysfunction as emerging mechanisms of nanomaterial toxicity (2012, background): “Currently, the most widely accepted paradigms of nanomaterial toxicity are oxidative stress and inflammation, but the underlying mechanisms are poorly defined [1].”
- Nanoparticles as Novel Elicitors to Improve Bioactive Compounds in Plants (2021, background): “In animals and humans, several risks are related to the safety of NPs which are associated with toxicity and can potentially cause inflammation, oxide stress, DNA damage, proteins damage, carcinogenesis, fibrosis and cell death [102–104].”