• Odie Beyer posted an update 1 week, 2 days ago

    C2C12 cells are mouse myoblast cells obtained from C3H mice. C2C12 cells are useful to study the expression of various proteins, and to explore mechanistic pathways. In addition, they are useful to study the differentiation of myoblast and osteoblast (Yaffe and Saxel, 1977). Our previous studies reported the cytotoxicity of ZnO nanoparticles on antioxidant enzyme activities and mRNA expression in the co-cultured C2C12 and 3T3-L1 cells (Muthuraman et al., 2015), and the dose-dependent effect of ZnO nanoparticles on oxidative stress, and antioxidant enzyme activity in adipocytes (Muthuraman et al., 2014). However, there are no reports on the effect of ZnO nanoparticles on the ALT, AST, ALP and LDH expressions in C2C12 cells. Therefore, the study is unique, and helps to understand the cytotoxicity of ZnO nanoparticle in C2C12 cells.Materials and methodsZnO nanoparticles (35nm particle size) were purchased from Sigma-Aldrich Chemical Co. (St. Louis, MO, USA). Laboratory wares were purchased from Falcon Lab ware (Becton-Dickinson, Franklin Lakes, NJ, USA). C2C12 cells (mouse, muscle) were purchased from ATCC.ResultsDiscussionZnO nanoparticles have been widely used in food products and in biomedical applications (Van Tassel and Goldman, 2011).Copper oxide nanoparticles showed dose-dependent cytotoxicity and oxidative stress in the airway epithelial cells. TiO2 nanoparticles produced oxidative stress and apoptosis in animal cells (Shukla et al., 2013). Reduced zinc concentration are associated with several metabolic and antioxidant enzymes (Kumar et al., 2011). High level of zinc is essential for cells and zinc is a component of many enzymes and transcription factors (Boreiko, 2010). Alteration of cellular zinc homeostasis associated with loss of viability, oxidative stress and dysfunction of mitochondria (Kao et al., 2012). Deng et al. (2009) reported that the ZnO nanoparticles caused neural stem cell toxicity in the culture medium. pH-triggered intracellular release of ionic Zn2+ is responsible for the cytotoxicity of ZnO nanowires (Müller et al., 2010). The adipose tissue expansion and adipocyte enlargement are associated with oxidative stress (Gregor and Hotamisligil, 2007). ZnO nanoparticles administration in mice showed its tissue distribution in the liver, spleen, kidneys and adipose tissue (Li et al., 2012). Elevated zinc level in the liver, adipose tissue and pancreas following MK-1775 manufacturer (Umrani and Paknikar, 2014), induction of oxidative stress, DNA damage and cell death was also reported (Kumar et al., 2011).Cytotoxicity of ZnO nanoparticles is due to their increased solubility. High concentration of metal oxide nanoparticles in the environment and food chain may affect human health (De Berardis et al., 2010). Increase of inflammation in the lymph nodes, the cells involved in the inflammatory reaction is due to nanoparticles (Qian, 2011; Su et al., 2009). Enzymatic peroxidation of fatty acids leads to the generation of the reactive oxygen species (Cohen et al., 2011). ROS is derived from mitochondria and endoplasmic reticulum (Wang and Joseph, 1999). The cells are affected when exposed to a higher concentration of reactive oxygen species (Dawei et al., 2010). ZnO nanoparticles are not toxic at low concentration, but at higher concentration increase ROS through increased MDA content (Syama et al., 2013). In our previous study, MDA content was altered significantly even at low concentrations of ZnO nanoparticles. LDH was present in adipose tissues of rat, and their distribution was significantly altered by metabolic stress (Moore and Yontz, 1969), increased LDH activity was reported in H1355 cells (Kao et al., 2012). Our results showed that the ZnO nanoparticles increase LDH activity in cells.AcknowledgementsIntroductionReactive oxygen species (ROS) are the endogenous free radicals of normal cellular metabolism. In living organisms, moderate concentrations of ROS benefit physiological functions such as intra-cellular signaling, cellular defense against infective agents, and induction of a mitogenic response. However, the excessive productions of free radicals can cause cellular lipid peroxidation, protein degradation, and DNA mutation, resulting in several degenerative diseases, including inflammation, cardiovascular diseases, cancer, diabetes, and neurological disorders (Valko et al., 2007; Carvalho et al., 2014). Generally, all the organisms are well protected against free radical damage by endogenous oxidative enzymes, such as superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and catalase (CAT). However, these enzymes are commonly insufficient when it comes to completely preventing degenerative diseases and other health problems (Borneo et al., 2009; Soares et al., 2009). In addition, several non-enzymatic antioxidant compounds such as phenolics, ascorbic acid, tocopherol, glutathione and other dietary compounds play an important role in defending the body against free radical damage by scavenging or neutralizing the oxidizing molecules and maintaining redox balance (Tachakittirungrod et al., 2007). Recent studies have reported that the plant kingdom offers a wide range of natural antioxidant molecules including phenolic acids, flavonoids, and other secondary metabolites and they can also be used for the treatment of various human disorders (Slusarczyk et al., 2009).

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