Molecular mechanism of titanium dioxide nanoparticles-induced oxidative injury in the brain of mice

Ze, Yuguan; Zheng, Lei; Zhao, Xiaoyang; Shen, Guanghui; Sang, Xuezi; Su, Junju; Guan, Ning; Zhu, Liyuan; Sheng, Lei; Hu, Renping; Cheng, Jie; Cheng, Zhe; Sun, Qingqing; Wang, Ling; Hong, Fashui

doi:10.1016/j.chemosphere.2013.01.094

Cited by 101 publications

(73 citation statements)

References 60 publications

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“…The activation of MAPK signaling molecules could ultimately activate the transcription factor NF-κB, 73 suggesting that SiNP-induced upregulated NF-κB expression may occur via the MAPK-Nrf2 signaling pathway. It has been confirmed that the activation of NF-κB and induction of HO-1 via the p38-Nrf2 signaling pathway are involved in oxidative stress induced by ceria NPs, 74 the ERK-Nrf2 pathway in that by SiNPs in human bronchial epithelial cells, 58 the p38-Nrf2 pathway in the oxidative damage induced by TiO 2 NPs, 75,76 and the p53 pathway in oxidative stress by ZnO NPs. 77 Additionally, NF-κB is a known modulator of inflammation, and its activation is responsive to various oxidant stimuli.…”

mentioning

confidence: 81%

Silica nanoparticles induce oxidative stress, inflammation, and endothelial dysfunction in vitro via activation of the MAPK/Nrf2 pathway and nuclear factor-κB signaling

Guo¹,

Xia²,

Niu³

et al. 2015

IJN

211

126

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Despite the widespread application of silica nanoparticles (SiNPs) in industrial, commercial, and biomedical fields, their response to human cells has not been fully elucidated. Overall, little is known about the toxicological effects of SiNPs on the cardiovascular system. In this study, SiNPs with a 58 nm diameter were used to study their interaction with human umbilical vein endothelial cells (HUVECs). Dose- and time-dependent decrease in cell viability and damage on cell plasma-membrane integrity showed the cytotoxic potential of the SiNPs. SiNPs were found to induce oxidative stress, as evidenced by the significant elevation of reactive oxygen species generation and malondialdehyde production and downregulated activity in glutathione peroxidase. SiNPs also stimulated release of cytoprotective nitric oxide (NO) and upregulated inducible nitric oxide synthase (NOS) messenger ribonucleic acid, while downregulating endothelial NOS and ET-1 messenger ribonucleic acid, suggesting that SiNPs disturbed the NO/NOS system. SiNP-induced oxidative stress and NO/NOS imbalance resulted in endothelial dysfunction. SiNPs induced inflammation characterized by the upregulation of key inflammatory mediators, including IL-1β, IL-6, IL-8, TNFα, ICAM-1, VCAM-1, and MCP-1. In addition, SiNPs triggered the activation of the Nrf2-mediated antioxidant system, as evidenced by the induction of nuclear factor-κB and MAPK pathway activation. Our findings demonstrated that SiNPs could induce oxidative stress, inflammation, and NO/NOS system imbalance, and eventually lead to endothelial dysfunction via activation of the MAPK/Nrf2 pathway and nuclear factor-κB signaling. This study indicated a potential deleterious effect of SiNPs on the vascular endothelium, which warrants more careful assessment of SiNPs before their application.

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mentioning

confidence: 81%

Silica nanoparticles induce oxidative stress, inflammation, and endothelial dysfunction in vitro via activation of the MAPK/Nrf2 pathway and nuclear factor-κB signaling

Guo¹,

Xia²,

Niu³

et al. 2015

IJN

211

126

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“…The characteristics of anatase TiO 2 NPs were described in detail in the previous reports [33,49]. Briefly, the average particle size of anatase TiO 2 NPs was approximately 5.5 nm, while the surface area was 174.8 m 2 /g, the mean hydrodynamic diameters of anatase TiO 2 NPs in hydroxypropylmethylcellulose (HPMC) solvent ranged from 208 to 330 nm (mainly 294 nm) and the ζ potential after 24 h incubation was 9.28 mV [32,49].…”

Section: Methodsmentioning

confidence: 99%

“…The photocatalytic properties of TiO 2 NPs have been proved to raise various issues with respect to its poisonous impacts in the lungs [11][12][13][14], livers [15][16][17][18][19][20][21], kidneys [22][23][24][25], spleens [26][27][28][29], brains [30][31][32][33][34][35][36] and hearts [37,38] of animals.…”

Section: Introductionmentioning

confidence: 99%

Decreased spermatogenesis led to alterations of testis-specific gene expression in male mice following nano-TiO2 exposure

Hong

Zhao

et al. 2015

Journal of Hazardous Materials

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“…Furthermore, exposure to TiO 2 NPs through intranasal administration has been shown to lead to the activation of HO-1 through the p38-Nrf-2 signaling pathway in mice, subsequently leading to ROS accumulation; the oxidation of lipids, proteins, and DNA; and brain injury. 117 …”

Section: Activated Cell-signaling Pathwaysmentioning

confidence: 99%

Central nervous system toxicity of metallic nanoparticles

Feng¹,

Chen²,

Zhang³

et al. 2015

IJN

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Nanomaterials (NMs) are increasingly used for the therapy, diagnosis, and monitoring of disease- or drug-induced mechanisms in the human biological system. In view of their small size, after certain modifications, NMs have the capacity to bypass or cross the blood–brain barrier. Nanotechnology is particularly advantageous in the field of neurology. Examples may include the utilization of nanoparticle (NP)-based drug carriers to readily cross the blood–brain barrier to treat central nervous system (CNS) diseases, nanoscaffolds for axonal regeneration, nanoelectromechanical systems in neurological operations, and NPs in molecular imaging and CNS imaging. However, NPs can also be potentially hazardous to the CNS in terms of nano-neurotoxicity via several possible mechanisms, such as oxidative stress, autophagy, and lysosome dysfunction, and the activation of certain signaling pathways. In this review, we discuss the dual effect of NMs on the CNS and the mechanisms involved. The limitations of the current research are also discussed.

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Molecular mechanism of titanium dioxide nanoparticles-induced oxidative injury in the brain of mice

Cited by 101 publications

References 60 publications

Silica nanoparticles induce oxidative stress, inflammation, and endothelial dysfunction in vitro via activation of the MAPK/Nrf2 pathway and nuclear factor-κB signaling

Silica nanoparticles induce oxidative stress, inflammation, and endothelial dysfunction in vitro via activation of the MAPK/Nrf2 pathway and nuclear factor-κB signaling

Decreased spermatogenesis led to alterations of testis-specific gene expression in male mice following nano-TiO2 exposure

Central nervous system toxicity of metallic nanoparticles

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Molecular mechanism of titanium dioxide nanoparticles-induced oxidative injury in the brain of mice

Cited by 101 publications

References 60 publications

Silica nanoparticles induce oxidative stress, inflammation, and endothelial dysfunction in vitro via activation of the MAPK/Nrf2 pathway and nuclear factor-&kappa;B signaling

Silica nanoparticles induce oxidative stress, inflammation, and endothelial dysfunction in vitro via activation of the MAPK/Nrf2 pathway and nuclear factor-&kappa;B signaling

Decreased spermatogenesis led to alterations of testis-specific gene expression in male mice following nano-TiO2 exposure

Central nervous system toxicity of metallic nanoparticles

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Silica nanoparticles induce oxidative stress, inflammation, and endothelial dysfunction in vitro via activation of the MAPK/Nrf2 pathway and nuclear factor-κB signaling

Silica nanoparticles induce oxidative stress, inflammation, and endothelial dysfunction in vitro via activation of the MAPK/Nrf2 pathway and nuclear factor-κB signaling