Titanium Dioxide (Tio2) Nanoparticles Induced ROS Generation and its Effect on Cellular Antioxidant Defense in WRL-68 Cell
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چکیده
Titanium dioxide nanoparticles (TIO2 NPs) have been widely used in manufacturing [1-4], in the environment to decontaminate air, soil, and water, and more recently in consumer products, car materials, and rubber [5,6]. Such widespread use and toxicological studies carried out in the last 10 years have shown that TIO2 NPs caused oxidative stress-mediated toxicity in cells [7-10], alveolar macrophages [9,11], DNA [9,12], and neurological lesion [13]. However, the influences of TIO2 NPs on human health are quite uncertain and less known. Recently, the potential impacts of nanoparticles on humans and the environment have greatly attracted the attention of scientists, industries, and regulatory issues of governments [8,14,15]. Numerous scientists’ work has given one main mechanism that the adverse health effects of TIO2 NPs are caused by oxidative stress [8,16]. They revealed that oxidative stress occurs when reactive oxygen species (ROS) disrupt the balance between oxidative pressure and antioxidant defense. ROS (such as hydroxyl radical, superoxide, etc.) could be produced by photo-activated, some chemicals on the particle surface, or a consequence of the interaction between particles and cellular components [16,17]. The mitochondria are the target of TIO2 NPs that have been phagocytosed by cells as well as a source for ROS production, and the disruption of mitochondria would also lead to the increase in ROS production, then the decrease of mitochondrial membrane potential and activation by apoptosis. Furthermore, ROS can also cause damage to protein, lipids, and DNA in cells. However, some studies have reported anatase-TIO2 NPs to be more biologically active than rutile-TIO2 NPs in terms of cytotoxicity [18]. It was demonstrated [19] that pure anataseTIO2 NPs induce cell necrosis and membrane leakage, but do not generate ROS. In contrast, rutile-TIO2 NPs initiate apoptosis through the formation of ROS. In previous study we have reported that CuO nano particals can leads to hyper methylation of promoter sequence of catalase thus lead to epigentic gene sequencing. In the present study we evaluate adverse consequence of TIO2 Nps on epigenetic gene silencing of catalase enzyme in WRL-68, human hepatic cell line.
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