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Redox interactions and genotoxicity of metal-based nanoparticles: A comprehensive review.
Mortezaee, Keywan; Najafi, Masoud; Samadian, Hadi; Barabadi, Hamed; Azarnezhad, Asaad; Ahmadi, Amirhossein.
Affiliation
  • Mortezaee K; Department of Anatomy, School of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran.
  • Najafi M; Radiology and Nuclear Medicine Department, School of Paramedical Sciences, Kermanshah University of Medical Sciences, Kermanshah, Iran. Electronic address: najafi_ma@yahoo.com.
  • Samadian H; Pharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran. Electronic address: h30samadiyan@gmail.com.
  • Barabadi H; Department of Pharmaceutical Biotechnology, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
  • Azarnezhad A; Cellular and Molecular Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran.
  • Ahmadi A; Pharmaceutical Sciences Research Center, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran. Electronic address: Amirhossein_pharma@yahoo.com.
Chem Biol Interact ; 312: 108814, 2019 Oct 01.
Article in En | MEDLINE | ID: mdl-31509734
Nanotechnology is a growing science that may provide several new applications for medicine, food preservation, diagnostic technologies, and sanitation. Despite its beneficial applications, there are several questions related to the safety of nanomaterials for human use. The development of nanotechnology is associated with some concerns because of the increased risk of carcinogenesis following exposure to nanomaterials. The increased levels of reactive oxygen species (ROS) that are due to exposure to nanoparticles (NPs) are primarily responsible for the genotoxicity of metal NPs. Not all, but most metal NPs are able to directly produce free radicals through the release of metal ions and through interactions with water molecules. Furthermore, the increased production of free radicals and the cell death caused by metal NPs can stimulate reduction/oxidation (redox) reactions, leading to the continuous endogenous production of ROS in a positive feedback loop. The overexpression of inflammatory mediators, such as NF-kB and STATs, the mitochondrial malfunction and the increased intracellular calcium levels mediate the chronic oxidative stress that occurs after exposure to metal NPs. In this paper, we review the genotoxicity of different types of metal NPs and the redox mechanisms that amplify the toxicity of these NPs.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Oxidative Stress / Metal Nanoparticles Limits: Animals / Humans Language: En Journal: Chem Biol Interact Year: 2019 Document type: Article Affiliation country: Iran Country of publication: Ireland

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Oxidative Stress / Metal Nanoparticles Limits: Animals / Humans Language: En Journal: Chem Biol Interact Year: 2019 Document type: Article Affiliation country: Iran Country of publication: Ireland