ZnO nanoparticle-induced oxidative stress triggers apoptosis by activating JNK signaling pathway in cultured primary astrocytes

Wang, Jieting; Deng, Xiaobei; Zhang, Fang; Chen, Deliang; Ding, Wenjun

doi:10.1186/1556-276x-9-117

Cited by 152 publications

(106 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For instance, the ZnO NP-astrocyte interaction was reported to induce an oxidative stress that could trigger cell apoptosis by activating the JNK signaling pathway in cultured primary astrocytes. 107 A similar finding was observed in the interactions between superparamagnetic iron oxide NPs and astrocytes. 108 Mixed glial cultures have often been established from the cerebral cortices of neonatal Sprague-Dawley rats and purified astrocytes.…”

Section: Neurotoxicity On Glial Cells or Neurogliasupporting

confidence: 68%

Application of dental nanomaterials: potential toxicity to the central nervous system

Feng¹,

Chen²,

Wang³

et al. 2015

IJN

View full text Add to dashboard Cite

Nanomaterials are defined as materials with one or more external dimensions with a size of 1–100 nm. Such materials possess typical nanostructure-dependent properties (eg, chemical, biological, optical, mechanical, and magnetic), which may differ greatly from the properties of their bulk counterparts. In recent years, nanomaterials have been widely used in the production of dental materials, particularly in light polymerization composite resins and bonding systems, coating materials for dental implants, bioceramics, endodontic sealers, and mouthwashes. However, the dental applications of nanomaterials yield not only a significant improvement in clinical treatments but also growing concerns regarding their biosecurity. The brain is well protected by the blood–brain barrier (BBB), which separates the blood from the cerebral parenchyma. However, in recent years, many studies have found that nanoparticles (NPs), including nanocarriers, can transport through the BBB and locate in the central nervous system (CNS). Because the CNS may be a potential target organ of the nanomaterials, it is essential to determine the neurotoxic effects of NPs. In this review, possible dental nanomaterials and their pathways into the CNS are discussed, as well as related neurotoxicity effects underlying the in vitro and in vivo studies. Finally, we analyze the limitations of the current testing methods on the toxicological effects of nanomaterials. This review contributes to a better understanding of the nano-related risks to the CNS as well as the further development of safety assessment systems.

show abstract

Section: Neurotoxicity On Glial Cells or Neurogliasupporting

confidence: 68%

Application of dental nanomaterials: potential toxicity to the central nervous system

Feng¹,

Chen²,

Wang³

et al. 2015

IJN

View full text Add to dashboard Cite

show abstract

“…Few studies in literature have documented the biochemical effects of Cu, CuO and ZnO NPs on earthworms in urban soils. The concentrations of NPs found to exhibit adverse effects on earthworms in artificial soils or natural soils tend to be several orders of magnitude lower [32,58,59] than what has been found in this study and other similar studies elsewhere [33,46]. These differences could be due to differences in specific soil characteristics.…”

Section: Hydrogen Peroxidecontrasting

confidence: 60%

Investigating the Toxicity of Cu, CuO and ZnO Nanoparticles on Earthworms in Urban Soils

Mwaanga¹,

Mbulwe²,

Shumbula³

et al. 2017

J Pollut Eff Cont

View full text Add to dashboard Cite

Even though some studies have shown that copper (Cu), copper oxide (CuO) and zinc oxide (ZnO) nanoparticles (NPs) are toxic to a number of organisms, fewer studies have investigated toxicity of these NPs in actual soils. This study investigated the effect of Cu, CuO and ZnO NPs in both urban and artificial soils. The aim was to examine the differences on these NPs' ability to cause oxidative stress to organisms in urban and artificial soils. Earthworms, Eisenia fetida, (2 months old) were exposed to varying concentrations of NPs and bulk materials (used for comparison purposes) of Cu, CuO and ZnO ranging from 100-500 mg/kg, 100-4000 mg/kg and 100-4000 mg/kg, respectively, for 14 days, for each soil type. Superoxide dismutase (SOD), reduced glutathione (GSH) and hydrogen peroxide (H 2 O 2 ) were measured at the end of exposure period. The accumulation of Cu and Zn in the earthworm tissues was measured using AAS. In urban soils, SOD, GSH and H2O2 all showed an initial increase as the concentration of NPs increased and but decreased at higher concentrations. Similar results for bulk materials were observed, though

show abstract

“…It has been reported that NPsinduced ROS production and oxidative stress through the MAPK pathway regulates apoptosis. [35][36][37] MAPK plays an essential role in modulating the functions of pro-and antiapoptotic proteins located in mitochondria. For example, JNK has been shown to be critically required for the release of cytochrome c from mitochondria.…”

Section: Discussionmentioning

confidence: 99%

Amorphous silica nanoparticles trigger vascular endothelial cell injury through apoptosis and autophagy via reactive oxygen species-mediated MAPK/Bcl-2 and PI3K/Akt/mTOR signaling

Guo¹,

Yang²,

Li³

et al. 2016

IJN

195

111

View full text Add to dashboard Cite

Environmental exposure to silica nanoparticles (SiNPs) is inevitable due to their widespread application in industrial, commercial, and biomedical fields. In recent years, most investigators focus on the evaluation of cardiovascular effects of SiNPs in vivo and in vitro. Endothelial injury and dysfunction is now hypothesized to be a dominant mechanism in the development of cardiovascular diseases. This study aimed to explore interaction of SiNPs with endothelial cells, and extensively investigate the exact effects of reactive oxygen species (ROS) on the signaling molecules and cytotoxicity involved in SiNPs-induced endothelial injury. Significant induction of cytotoxicity as well as oxidative stress, apoptosis, and autophagy was observed in human umbilical vein endothelial cells following the SiNPs exposure ( P <0.05). The oxidative stress was induced by ROS generation, leading to redox imbalance and lipid peroxidation. SiNPs induced mitochondrial dysfunction, characterized by membrane potential collapse, and elevated Bax and declined bcl-2 expression, ultimately leading to apoptosis, and also increased number of autophagosomes and autophagy marker proteins, such as LC3 and p62. Phosphorylated ERK, PI3K, Akt, and mTOR were significantly decreased, but phosphorylated JNK and p38 MAPK were increased in SiNPs-exposed endothelial cells. In contrast, all of these stimulation phenomena were effectively inhibited by N -acetylcysteine. The N -acetylcysteine supplement attenuated SiNPs-induced endothelial toxicity through inhibition of apoptosis and autophagy via MAPK/Bcl-2 and PI3K/Akt/mTOR signaling, as well as suppression of intracellular ROS property via activating antioxidant enzyme and Nrf2 signaling. In summary, the results demonstrated that SiNPs triggered autophagy and apoptosis via ROS-mediated MAPK/Bcl-2 and PI3K/Akt/mTOR signaling in endothelial cells, and subsequently disturbed the endothelial homeostasis and impaired endothelium. Our findings may provide experimental evidence and explanation for cardiovascular diseases triggered by SiNPs. Furthermore, results hint that the application of antioxidant may provide a novel way for safer use of nanomaterials.

show abstract

ZnO nanoparticle-induced oxidative stress triggers apoptosis by activating JNK signaling pathway in cultured primary astrocytes

Cited by 152 publications

References 60 publications

Application of dental nanomaterials: potential toxicity to the central nervous system

Application of dental nanomaterials: potential toxicity to the central nervous system

Investigating the Toxicity of Cu, CuO and ZnO Nanoparticles on Earthworms in Urban Soils

Amorphous silica nanoparticles trigger vascular endothelial cell injury through apoptosis and autophagy via reactive oxygen species-mediated MAPK/Bcl-2 and PI3K/Akt/mTOR signaling

Contact Info

Product

Resources

About