&lt;p&gt;Zinc Oxide Nanoparticles Induce Ferroptotic Neuronal Cell Death in vitro and in vivo&lt;/p&gt;

Qin, Xia; Tang, Qianghu; Jiang, Xuejun; Zhang, Jun; Wang, Bin; Liu, Xuemei; Zhang, Yandan; Zou, Zhen; Chen, Chengzhi

doi:10.2147/ijn.s250367

Cited by 42 publications

(24 citation statements)

References 60 publications

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“…The failure to do so indicates an error in the reference memory while the working memory is assessed when the mouse made an entry to each arm a single time. Re‐entry into the arms with no food reward would be considered as working memory error [ 43 ].…”

Section: Resultsmentioning

confidence: 99%

Behavioural alterations induced by chronic exposure to 10 nm silicon dioxide nanoparticles

Jarrar

Al‐Doaiss

Shati

et al. 2021

IET Nanobiotechnology

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Silicon dioxide nanoparticles (SiO 2 NPs) are widely invested in medicine, industry, agriculture, consuming products, optical imaging agents, cosmetics, and drug delivery. However, the toxicity of these NPs on human health and the ecosystem have not been extensively studied and little information is available about their behavioural toxicities. The current study aimed to find out the behavioural alterations that might be induced by chronic exposure to 10 nm SiO 2 NPs. BALB/C mice were subjected to 36 injections of SiO 2 NPs (2 mg/kg Bw) and subjected to 11 neurobehavioural tests: elevated plus-maze test, elevated zero-maze test, multiradial maze test, open field test, hole-board test, light-dark box test, forced swimming test, tail-suspension test, Morris water-maze test, Y-maze test and multiple T-maze test. Treated mice demonstrated anxiety-like effect, depression tendency, behavioural despair stress, exploration and locomotors activity reduction with error induction in both reference and working memories. The findings may suggest that silica NPs are anxiogenic and could aggravate depression affecting memory, learning, overall activity and exploratory behaviour. Moreover, the findings may indicate that these nanomaterials (NMs) may induce potential oxidative stress in the body leading to neurobehavioural alterations with possible changes in the vital organ including the central nervous system.This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Section: Resultsmentioning

confidence: 99%

Behavioural alterations induced by chronic exposure to 10 nm silicon dioxide nanoparticles

Jarrar

Al‐Doaiss

Shati

et al. 2021

IET Nanobiotechnology

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“…A previous study on ICH suggested that the JNK pathway could be initiated, with upregulation of pJNK (Hibi et al, 1993;Pei et al, 2016). Other studies indicated that JNK is involved in ferroptotic cell death in mouse cortex and PC-12 cells (Qin et al, 2020). TNFAIP3, an important anti-inflammatory factor, can repress the expression of inflammatory NF-κB signaling and promote cell survival (Catrysse et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics Analysis Identifies Potential Ferroptosis Key Genes in the Pathogenesis of Intracerebral Hemorrhage

Liu

Cui

et al. 2021

Front. Neurosci.

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Intracerebral hemorrhage (ICH) is a dangerous neurological disease. The mechanism of ferroptosis in ICH remains unclear. Using bioinformatics analysis, we aimed to identify the key molecules involved in ferroptosis and provide treatment targets for ICH to further explore the mechanism of ferroptosis in ICH. GSE24265 was downloaded from the Gene Expression Omnibus (GEO) dataset and intersected with ferroptosis genes. A total of 45 differentially expressed genes (DEGs) were selected, most of which were involved in the TNF signaling pathway and oxidative stress response. Key modules constructed by the protein–protein interaction (PPI) network analysis and screening of genes related to the TNF signaling pathway led to the confirmation of the following genes of interest: MAPK1, MAPK8, TNFAIP3, ATF4, and SLC2A1. Moreover, MAPK1 was one of the key genes related to TNF signaling and oxidative stress, and it may play an important role in ferroptosis after cerebral hemorrhage. The MAPK1-related molecules included hsa-miR-15b-5P, hsa-miR-93-5P, miR-20b-5p, SNHG16, XIST, AC084219.4, RP11-379K17.11, CTC-444N24.11, GS1-358P8.4, CTB-89H12.4, RP4-773N10.5, and FGD5-AS1. We also generated a hemorrhage rat model, which was used to conduct exercise intervention in ICH rats, and qRT-PCR was used to assess the expression levels of our genes of interest. The mRNA levels after cerebral hemorrhage showed that MAPK1, ATF4, SLC2A1, and TNFAIP3 were upregulated, whereas MAPK8 was downregulated. Treadmill training increased the expression of anti-inflammatory molecules TNFAIP3 and SLC2A1 and reduced the expression of MAPK1, ATF4, and MAPK8, indicating that treadmill training may be utilized as antioxidant therapy to decrease neuronal ferroptosis. The results of this study indicated that the MAPK1-related mRNA–miRNA–lncRNA interaction chain could be potentially employed as a biomarker of the inception and progression of ferroptosis after cerebral hemorrhage.

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“…Zinc oxide nanoparticles (ZnONPs) interfere with iron homeostasis and ROS production, ultimately leading to ferroptosis 30 . The ferroptosis induced by ZnONPs is JNK and p53 dependent, as JNK, inhibitor and p53 siRNA abrogate this effect 30,31 . Besides, other nanomaterials such as Al 2 O 3 , Fe 3 O 4 , and TiO 2 also cause intracellular Fe 2+ elevation in HUVECs 30 .…”

Section: Discussionmentioning

confidence: 99%

Nickel oxide nanoparticles induce apoptosis and ferroptosis in airway epithelial cells via ATF3

Liu

Cheng

et al. 2022

Environmental Toxicology

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Exposure to nickel oxide nanoparticles (NiONPs), which have been widely produced and applied in industry, leads to adverse pulmonary and systemic effects. The aim of this study is to investigate the involvement of apoptosis and ferroptosis in NiONPsinduced acute lung injury (ALI). Intratracheal instillation of NiONPs into mice elevated the levels of pro-inflammatory cytokines, neutrophils, and proteins in the bronchoalveolar lavage fluid, and triggered apoptosis and ferroptosis in the lung tissues. Consistently, NiONPs-induced apoptosis and ferroptosis were observed in in vitro experiments using human lung epithelial cells. Activating transcription factor 3 (ATF3), a stress-inducible transcription factor, was upregulated by NiONPs exposure in both murine lung tissues and human lung epithelial cells. Moreover, human lung epithelial cells with ATF3 deficiency exhibited a lower level of apoptosis and ferroptosis when exposed to NiONPs. Collectively, our findings demonstrated that ATF3 was responsive to NiONPs exposure, and promoted NiONPs-induced apoptosis and ferroptosis in lung epithelial cells, indicating that ATF3 is a potential biomarker and therapeutic target for NiONPs-associated ALI.

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<p>Zinc Oxide Nanoparticles Induce Ferroptotic Neuronal Cell Death in vitro and in vivo</p>

Cited by 42 publications

References 60 publications

Behavioural alterations induced by chronic exposure to 10 nm silicon dioxide nanoparticles

Behavioural alterations induced by chronic exposure to 10 nm silicon dioxide nanoparticles

Bioinformatics Analysis Identifies Potential Ferroptosis Key Genes in the Pathogenesis of Intracerebral Hemorrhage

Nickel oxide nanoparticles induce apoptosis and ferroptosis in airway epithelial cells via ATF3

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