A Brief Overview to the Toxicity Mechanisms of Different Nanoparticles

Mehdi Ghobadian*

Department of developmental Biology, Kharazmi University, Tehran, Iran

Corresponding Author:
Mehdi Ghobadian
Department of developmental Biology
Faculty of Biological Sciences
Kharazmi University, Tehran, Iran
Tel: 98 21 8832 9220
E-mail: [email protected]

Received date: June 21, 2016; Accepted date: June 22, 2016; Published date: June 24, 2016

Citation: Ghobadian M. A Brief Overview to the Toxicity Mechanisms of Different Nanoparticles. J Clin Dev Biol. 2016, 1:3.

 
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Editorial

Nanoparticles have at least one dimension less than 100 nm and their components demonstrate unusual features based on quantum mechanics, rather than macroscopic Newtonian mechanics [1]. Their novel physicochemical, thermal, and electrical properties facilitate their application in various fields, thereby increasing the possibility for human and environmental contact with these nanoparticles [2]. Human skin, lungs, and the gastro-intestinal tract are the most likely points of entry for natural or anthropogenic nanoparticles [3]. There are some studies that have investigated the mechanisms of toxicity of different nanoparticles in human, zebrafish and other organisms. Krishnamoorthy et al. [4] in mechanistic investigation of Magnesium Oxide Nanoparticles (MgONPs) toxicity toward cancer cells, confirmed the role of apoptosis in cell death due to MgONPs exposure [4]. Also, their flow cytometric measurments showed that the toxicity of MgONPs is attributed to the generation of Reactive Oxygen Species (ROS) [4]. In other study, Aerle et al. [5] evaluated the molecular mechanisms of toxicity of silver nanoparticles in zebrafish embryos. Their findings showed significant alterations in gene expression for all treatments and many of gene pathways affected, most notably those associated with oxidative phosphorylation and protein synthesis [5]. In a similar study, Thomas et al. [6] evaluated the toxicity of magnesium oxide nanoparticles in two freshwater fishes tilapia (Oreochromis mossambicus) and zebrafish (Danio rerio). Their results showed that there was a gradual and sporadic increase in the catalase activity. Also they confirmed that the specific activity of Glutathione-S-transferase increased significantly with an increase in the concentration of MgONPs [6]. In other study, zebrafish embryos exposed to chitosan nanoparticles showed an increased rate of cell death, high expression of ROS, as well as overexpression of heat shock protein 70 [7]. Pulmonary toxicity of MgONPs in rats were evaluated by Gelli et al. [8]. Their findings showed a dose-dependant increase in alkaline phosphatase and lactate dehydrogenase activity that was observed in bronchoalveolar lavage fluid [8]. Ghobadian et al. [9] confirmed that MgONPs induced cellular apoptosis and intracellular ROS in zebrafish larvae following embryoniv exposure to these nanoparticles [9]. Clemente et al. [10] in toxicity assessment of TiO2 nanoparticles in zebrafish embryos under different exposure conditions revealed that alterations in the activities of catalase and Glutathione-S-transferase were indicative of oxidative stress [10]. Moreover both in vivo and in vitro studies have shown that nanoparticles of various compositions create ROS to damage cells by peroxidizing lipids, altering proteins, disrupting DNA, interfering with signaling functions, and modulating gene transcription [10]. In general it can be concluded that various nanoparticles with different mechanisms disrupt cell function and exert their toxic effects.

References

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