Titanium dioxide nanoparticles induce apoptosis through the JNK/p38-caspase-8-Bid pathway in phytohemagglutinin-stimulated human lymphocytes

Kang, Su Jin; Kim, Byeong Mo; Lee, Young Joon; Hong, Sung Hee; Chung, Hai Won

doi:10.1016/j.bbrc.2009.06.097

Cited by 89 publications

(53 citation statements)

References 22 publications

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“…For example, some studies have shown that apoptosis is triggered by TiO 2 NPs. Kang et al (2009) and Zhao et al (2009) reported that TiO 2 NP-induced apoptosis is mediated by the caspase-8/t-Bid pathway, whereas Shi et al (2010) did not. The p53 pathway mediates TiO 2 NPs-induced apoptosis (Kang et al, 2008;Shi et al, 2010;Wu et al, 2010).…”

Section: It Is Critical To Assess Potential Impacts Of Nps Onmentioning

confidence: 99%

Silver nanoparticles induce p53-mediated apoptosis in human bronchial epithelial (BEAS-2B) cells

et al. 2014

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-Deregulated apoptosis has been associated with many lung diseases. Although many studies have reported the apoptotic effects exhibited by silver nanoparticles (Ag-NPs) in various circumstances, the apoptosis mechanism of Ag-NPs is unclear. We investigated oxidative stress and apoptosis in human normal bronchial epithelial (BEAS-2B) cells to elucidate the role of p53 in apoptosis by Ag-NPs. First, dispersion and stability of Ag-NPs improved using bronchial epithelial cell growth medium with 5% fetal bovine serum. Then, we observed oxidative stress in BEAS-2B cells exposed to Ag-NPs. Second, we carried out a cell death assay to measure DNA fragmentation as a biomarker of apoptosis. BEAS--mentation. We also found that apoptosis-related genes (caspase-3, Bax, and Bcl-2) were regulated by AgNPs, which was detected by mRNA and protein levels. These results suggest that Ag-NPs induced p53-Ag-NPs in pulmonary disease. Original ArticleThe Journal of Toxicological Sciences (J. Toxicol. Sci.) Vol.39, No.3, 401-412, 2014 Vol. 39 No. 3 401 lar and DNA damage (Risom et al., 2005). DNA damage induces extracellular and intracellular signals that trigger the onset of a signaling cascade with characteristic biochemical and morphological features, including nuclear condensation, membrane blebbing, and DNA fragmentation, leading ultimately to cell death (Johnson et al., 1996). This is called apoptosis, which is essential for the normal functioning and survival of multi-cellular organisms. However, deregulated apoptosis has been associated with many lung diseases because toxic contents are released from apoptotic cells unless the cells are quickly recognized or ingested by phagocytes (Pandya et al., 2006).The p53 gene regulates the apoptosis pathway (Korsmeyer, 1995;Yang and Duerksen-Hughes, 1998) and is tightly controlled through a complex series of events including translational regulation, interaction with regu--cations including multisite phosphorylation and acetylation (Giaccia and Kastan, 1998;Meek, 1999;Prives and Hall, 1999). In particular, phosphorylation of the serine-15 (Ser-15) residue due to DNA damage plays an important role in p53-mediated apoptosis (Dumaz and Meek, 1999;Siliciano et al., 1997;Unger et al., 1999). This activation of p53 leads to expression of its downstream effectors such as Bax, Bcl-2 and caspase-3, resulting in apoptosis (Martin and Elkon, 2004).In this study, we hypothesized that Ag-NPs induce apoptosis via the p53 signaling pathway in normal human lung bronchial epithelial (BEAS-2B) cells. Although many reports have shown apoptotic effects of Ag-NPs in various circumstances (Foldbjerg et al., 2009;Li et al., 2010;Miura and Shinohara, 2009;Piao et al., 2011), the were used to elucidate the role of p53 in apoptosis by Ag--sion of TiO 2 NPs improved by adding bovine serum albumin (BSA) or fetal bovine serum (FBS) to the medium (Ji et al., 2010). Thus, Ag-NPs were dispersed in bronchial epithelial growth medium (BEGM) with 5% FBS and were characterized. Then, we observed ROS generation...

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Section: It Is Critical To Assess Potential Impacts Of Nps Onmentioning

confidence: 99%

Silver nanoparticles induce p53-mediated apoptosis in human bronchial epithelial (BEAS-2B) cells

et al. 2014

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“…For example phytohemagglutininstimulated human lymphocytes during 24 h showed parp cleavage was activated by nano-TiO 2 [35]. On the contrary, we did not observe any apoptotic signature in TiO 2 -NPs treated cell groups ( Figure 3C).…”

Section: Discussionmentioning

confidence: 44%

Enhancing Antioxidant Cellular Defense by Using Quercetin Loaded TiO2 Nanoparticles in Swiss 3T3 Albino Mouse Fibroblast Cells

Birinci¹,

Niazi²,

Başağa³

2017

J Nanomed Nanotechnol

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Living organisms are continuously exposed to a wide variety of oxidative radicals. Therefore, there is a constant demand for exogenous antioxidant supply. In this regard, one of these exogenous antioxidants with well established potency, quercetin has been utilized in various formulations. Yet due to its poor water solubility, its extensive applications are limited so far. In this study, TiO 2 nanoparticles (TiO 2 -NPs) were employed to improve the cellular penetration of quercetin and to maximize its antioxidant effects on swiss 3T3 albino mouse fibroblast cells. Surfaces of TiO 2 -NPs were modified with Polyethylene glycol (PEG) that enabled better dispersion and enhanced biocompatibility. Toxicity of quercetin and quercetin loaded TiO 2 NPs (QL-TiO 2 -NPs) were evaluated in terms of cell morphology and measured with cell viability assay. For an in-depth cell viability analysis, key markers of apoptosis were investigated by immunoblotting analysis. As an indicator of apoptotic cell death, cleavage of caspase 3 (Cas 3) and poly (ADP-ribose) polymerase proteins (Parp) were detected in quercetin treated cells. Antioxidant capacity of quercetin in the form of QL-TiO 2 -NPs was measured in the cells in which generation of reactive oxygen species (ROS) and superoxide was induced by pyocyanin. Quantitative ROS measurements were confirmed with confocal microscopy. Further mechanistic insight on upregulation of NF-E2 related factor 2 (NRF2) pathway via QL-TiO 2 -NPs was also provided in an effort to validate its antioxidant defense. Target enzymes of NRF2, heme oxygenase-1 (HO-1), NAD(P)H: quinone oxydoreductase1 (NQO1) and superoxide dismutase1 (SOD1) expressions were increased in the model proposed. QL-TiO 2 -NPs allowed high bioavaliability of quercetin concentration and stability in the cell with maximum antioxidant capacity against formation of ROS without any cytotoxicity. Overall, this paper sheds light on how the efficiency of quercetin in a nanosystem can serve as a safe therapeutic candidate for breaking the vicious ROS cycle in the cell. Citation: Birinci Y, Niazi JH, Basaga H (2017) Enhancing Antioxidant Cellular Defense by Using Quercetin Loaded TiO 2 Nanoparticles in Swiss 3T3Albino Mouse Fibroblast Cells. J Nanomedic Nanotechnol S8: 001. doi:10.4172/2157-7439.S8-001Page 2 of 10 J Nanomedic Nanotechnol Nanotechnology: Challenges and Perspectives in Medicine ISSN: 2157-7439 JNMNT an open access journal 3T3 albino mouse fibroblast cells. Total cellular ROS and superoxide levels in treated cells were determined and compared with those of control cells. However, quercetin in a nanosystem shows maximum antioxidant activity by triggering NRF2 pathway, upregulating phase II antioxidant enzymes, heme oxygenase-1 (HO-1), NAD(P)H: quinone oxydoreductase1 (NQO1) and superoxide dismutase1 (SOD1). In summary, our study demonstrated that quercetin loaded TiO 2 -NPs served as an effective nanosystem for delivering quercetin to swiss 3T3 albino mouse fibroblast cells in vitro and provided protection against oxida...

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“…These studies afford correlative evidence, but also are designed to search new possibilities of tumor destruction [52]. Many in vitro experiments confirm the preventing role of Bcl-2 in apoptosis activating in different type of cancer [97].…”

Section: The Role Of P53 and Bcl-2 Family In Apoptosismentioning

confidence: 99%

“…However, in 50% of cancers the p53 gene is disrupted and losses its ability to bind to these proteins. Hence research is continuing on the use of synthetic inhibitors in preclinical and clinical study (Table 1.) [97]. The most of them determined the direction of future clinical development and are promising.…”

Section: The Role Of P53 and Bcl-2 Family In Apoptosismentioning

confidence: 99%

Apoptosis, Free Radicals and Antioxidant Defense in Antitumor Therapy

Kulbacka¹,

Saczko²,

Chwiłkowska³

et al. 2012

Antioxidant Enzyme

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Titanium dioxide nanoparticles induce apoptosis through the JNK/p38-caspase-8-Bid pathway in phytohemagglutinin-stimulated human lymphocytes

Cited by 89 publications

References 22 publications

Silver nanoparticles induce p53-mediated apoptosis in human bronchial epithelial (BEAS-2B) cells

Silver nanoparticles induce p53-mediated apoptosis in human bronchial epithelial (BEAS-2B) cells

Enhancing Antioxidant Cellular Defense by Using Quercetin Loaded TiO2 Nanoparticles in Swiss 3T3 Albino Mouse Fibroblast Cells

Apoptosis, Free Radicals and Antioxidant Defense in Antitumor Therapy

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