Role of NF‐<i>κ</i>B activation and Th1/Th2 imbalance in pulmonary toxicity induced by nano NiO

Chang, Xuhong; Zhu, An; Liu, Fangfang; Zou, Lin; Su, Li; Li, Sheng; Sun, Yuhao

doi:10.1002/tox.22329

Cited by 38 publications

(43 citation statements)

References 34 publications

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“…Thus, impaired redox balance may obviously lead to the activation of NF-κB. 39 Moreover, the generation of high levels of NO, followed by the rapid production of other reactive nitrogen species, which are the major components of oxidative stress, is often considered as an essential mechanism of nanomaterial toxicity. 40 Prolonged or excessive NO production has deleterious effects leading, among others, to serious endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

In vitro toxicity studies of biodegradable, polyelectrolyte nanocapsules

Karabasz¹,

Szczepanowicz²,

Cierniak³

et al. 2018

IJN

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BackgroundToxicity of nanomaterials is one of the most important factors limiting their medical application. Evaluation of in vitro nanotoxicity allows for the identification and elimination of most of the toxic materials prior to animal testing. The current knowledge of the possible side effects of biodegradable nanomaterials, such as liposomes and polymeric organic nanoparticles, is limited. Previously, we developed a potential drug delivery system in the form of nanocapsules with polyelectrolyte, biodegradable shells consisting of poly-l-lysine and poly-l-glutamic acid (PGA), formed by the layer-by-layer adsorption technique.MethodsHemolysis assay, viability tests, flow cytometry analysis of vascular cell adhesion molecule-1 expression on endothelium, analysis of nitric oxide production, measurement of intracellular reactive oxygen species levels, detection of antioxidant enzyme activity, and analysis of DNA damage with comet assay were performed to study the in vitro toxicity of nanocapsules.ResultsIn this work, we present the results of an in vitro analysis of toxicity of five-layer positively charged poly-l-lysine–terminated nanocapsules (NC5), six-layer negatively charged PGA-terminated nanocapsules (NC6) and five-layer PEGylated nanocapsules (NC5-PEG). PGA and polyethylene glycol (PEG) were used as two different “stealth” polymers. Of all the polyelectrolyte nanocapsules tested for blood compatibility, only cationic NC5 showed acute toxicity toward blood cells, expressed as hemolysis and aggregation. Neither NC6 nor NC5-PEG had proinflammatory activity evaluated through changes in the expression of NF-κB–dependent genes, iNOS and vascular cell adhesion molecule-1, induced oxidative stress, or promoted DNA damage in various cells.ConclusionOur studies clearly indicate that PGA-coated (negatively charged) and PEGylated polyelectrolyte nanocapsules do not show in vitro toxicity, and their potential as a drug delivery system may be safely studied in vivo.

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Section: Discussionmentioning

confidence: 99%

In vitro toxicity studies of biodegradable, polyelectrolyte nanocapsules

Karabasz¹,

Szczepanowicz²,

Cierniak³

et al. 2018

IJN

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“…Single intratracheal instillation of nano-NiO in rats induces oxidative stress, inflammatory response, collagen deposition, and apoptosis in lung tissues (6)(7)(8). In our previous studies, nano-NiO was demonstrated to result in lung lesions following intratracheal instillation for 6 weeks in rats and to enhance the nitrative stress and inflammatory response (9), an effect that was associated with nuclear factor-κB activation and T helper (Th)1/Th2 cell imbalance (10). Other reports have also demonstrated that nano-NiO induces toxicity in various cell lines, including human bronchial epithelial cells, type II human alveolar epithelial cells, human monocytes and mouse embryonic stem cells (11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

Role of oxidative stress in liver toxicity induced by nickel oxide nanoparticles in rats

Liu

Wang

et al. 2017

Mol Med Report

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The aim of the present study was to explore the role of oxidative stress in liver toxicity induced by nickel oxide nanoparticles (nano‑NiO) in rats. Male Wistar rats received saline (control), nano‑NiO [0.015, 0.06 or 0.24 mg/kg body weight (b.w.)] or micro‑NiO (0.24 mg/kg b.w.) by intratracheal instilling twice a week for 6 weeks. Liver tissues were then collected and examined for biomarkers of nitrative and oxidative stress, as well as mRNA expression of heme oxygenase (HO)‑1 and metallothionein (MT)‑1. The results demonstrated that the NiO exposure groups had increased liver wet weight and coefficient to body weight, as well as liver pathological changes, evidenced as cellular edema, hepatic sinus disappeara-nce and binucleated hepatocytes. The activities of total nitric oxide synthase and inducible nitric oxide synthase, and the nitric oxide content, were increased in the 0.24 mg/kg nano‑NiO group compared with the control group. The MT‑1 mRNA expression levels were downregulated, while HO‑1 mRNA was upregulated in the 0.24 mg/kg nano‑NiO exposure group compared with the control group. In addition, abnormal changes of hydroxyl radical, lipid peroxidation, catalase, glutathione peroxidase, total superoxide dismutase and total antioxidative capacity were observed in the liver tissues of the 0.24 mg/kg nano‑NiO exposure group, compared with the control group. The present results therefore indicated that nano‑NiO‑induced liver toxicity may be associated with nitrative and oxidative stress in rats.

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“…The average diameter of nano NiO suspended in 0.9% NaCl was 244.5 nm. Other details of physicochemical characteristic were presented in our previous studies …”

Section: Resultsmentioning

confidence: 99%

“…nano NiO group, and 0.24 mg/kg b.w. micro NiO group . Rats were intratracheally instilled samples suspension (1 mL/kg b.w.)…”

Section: Methodsmentioning

confidence: 99%

Nickel oxide nanoparticles induce hepatocyte apoptosis via activating endoplasmic reticulum stress pathways in rats

Chang

Liu

Tian

et al. 2017

Environmental Toxicology

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Nickel oxide nanoparticles (nano NiO) could induce hepatocyte apoptosis, while its potential mechanisms are unclear. This study aimed to explore the role of endoplasmic reticulum (ER) stress pathways in hepatocyte apoptosis induced by nano NiO. Male Wistar rats were administrated with nano NiO (0.015, 0.06, and 0.24 mg/kg b.w.) and micro NiO (0.24 mg/kg b.w.) by intratracheal instillation twice a week for 6 weeks. We measured the hepatocyte apoptosis levels by TdT-mediated dUTP nick-end labeling (TUNEL) staining, ER stress related gene and protein expression levels in rat liver. The results showed that the TUNEL positive cells increased after exposure nano NiO, hinting hepatocyte apoptosis. The up-regulated gene and protein levels of 78 kD glucose regulated protein and CCAAT/enhancer binding protein homologous protein suggested that nano NiO triggered ER stress. Nano NiO exposure contributed to the increased protein contents of inositol-requiring enzyme 1 (IRE-1)α, p-IRE-1α, X box protein-1S, pancreatic ER kinase (PERK), p-PERK, eukaryotic initiation factor-2 alpha (eIF-2α), p-eIF-2α, caspase-12, -9, and -3, implicating that nano NiO can activate the pathways of ER stress-mediated apoptosis. These findings indicate that the ER stress pathways may play an important role in hepatocyte apoptosis induced by nano NiO.

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Role of NF‐κB activation and Th1/Th2 imbalance in pulmonary toxicity induced by nano NiO

Cited by 38 publications

References 34 publications

In vitro toxicity studies of biodegradable, polyelectrolyte nanocapsules

In vitro toxicity studies of biodegradable, polyelectrolyte nanocapsules

Role of oxidative stress in liver toxicity induced by nickel oxide nanoparticles in rats

Nickel oxide nanoparticles induce hepatocyte apoptosis via activating endoplasmic reticulum stress pathways in rats

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