Nickel Oxide Nanoparticles Induced Transcriptomic Alterations in HEPG2 Cells

Saquib, Quaiser; Siddiqui, Maqsood A.; Ahmad, Javed; Ansari, Sabiha M.; Faisal, Mohammad; Wahab, Rizwan; Alatar, Abdulrahman A.; Al-Khedhairy, Abdulaziz A.; Musarrat, Javed

doi:10.1007/978-3-319-72041-8_10

Cited by 31 publications

(21 citation statements)

References 46 publications

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“…Previous studies indicated the NiO-NPs caused damage in lung and liver and induce pulmonary inflamations via reactive oxygen species (ROS) (Chang et al, 2017;Li et al, 2018;Marzban et al, 2017;Senoh et al, 2017;Shinohara et al, 2017;Yu et al, 2017;Dumala et al, 2018;Ogami et al, 2009). In vitro researches confirmed with the in vivo studies that the NiO-NPs induced an increase in ROS and caused oxidative damage in the cells (Abudayyak et al 2017a;Åkerlund et al, 2018;Di Bucchianico et al, 2018;Mohamed et al, 2018;Saquib et al, 2018). Previous data confirmed with our results; oxidative stress could be the mechansim underlying the cytoand genotoxicity induced by the NiO-NPs .…”

Section: Tablesupporting

confidence: 91%

“…The results indicated that apoptosis could be the main cell death pathway in exposure to NiO-NPs. De Bucciani et al (2018) and Saquib et al (2018) observed increase in the apoptotic cells in dose dependent manner (De Bucciani et al, 2018;Saquib et al, 2018). Similarly, Chang et al (2017b) indicated endoplasmic reticulum stress related apoptosis in rat exposed to NiO-NPs by intratracheal instillation (Chang et al, 2017b).…”

Section: Tablementioning

confidence: 96%

“…The NiO-NPs induced apoptosis by functional alterations in mitochondri and lysosome at 25-100 µg/mL (Ahmad et al, 2013) similar to our results. Previously, the changes of mRNA levels in the genes related to apoptosis pathway were reported (Ahamed et al, 2013;Saquib et al, 2018;Siddiqui et al, 2012). Duan et al (2015) investigated the impacts of NiO-NPs on sirtuin 1, a NAD-dependent deacetylase involved in apoptosis in human bronchial epithelial cells (BEAS-2B).…”

Section: Figurementioning

confidence: 99%

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Intestinal Epithelial Cell Toxicity Induced By Nickel Oxide Nanoparticles

Asadi¹,

Güzel²,

Özhan³

2019

tjps

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INTRODUCTION: The superior properties of nickel oxide nanoparticles (NiO-NPs) lead to wide uses in various fields; however, there has been little comprehensive knowledge about their toxicity, especially oral exposure. Because there was no study on the intestinal toxicity of NiO-NPs, the toxicity of The NiO-NPs (average size 15.0 nm) was investigated in Caco-2 (human intestinal epithelial) cells. METHODS: Following identification of their particle size distribution and cellular uptake potential, the risk of NiO-NPs' exposure have been evaluated with the crucial toxicity features including the cellular morphologic changes, the cyto-and genotoxic potentials, oxidative damage and apoptotic induction. RESULTS: According to our results, NiO-NPs caused 50% decrease in cell viability at 351.6 µg/mL, and induced DNA damage and oxidative damage at 30-150 µg/mL. It was observed that apoptosis could be the main cell death pathway at in intestinal cells exposed to NiO-NPs. DISCUSSION AND CONCLUSION: The exposure to NiO-NPs could be hazardous to the gastrointestinal system, the results should rise the concerns about using NiO-NPs in food-contacts appliance and NiO-NPs containing wastes. Further in vivo and in vitro research should be conducted to explain the specific mechanism of these particles and reduce their risk to the human.

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Section: Tablesupporting

confidence: 91%

Section: Tablementioning

confidence: 96%

Section: Figurementioning

confidence: 99%

See 1 more Smart Citation

Intestinal Epithelial Cell Toxicity Induced By Nickel Oxide Nanoparticles

Asadi¹,

Güzel²,

Özhan³

2019

tjps

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“…cerevisiae (Sousa, Soares, & Soares, 2018). The ability of NiO-NPs to induce apoptosis, DNA damage, oxidative stress and alterations in the transcriptome of human liver cells (HepG2) has been well documented (Saquib et al, 2018). De Carli et al (2018) depicted the genotoxicity and mutagenic potential of NiO-NPs by testing on Chinese hamster normal lung fibroblast cells and Drosophila melanogaster, respectively.…”

mentioning

confidence: 99%

Retracted: In vitro genotoxicity assessment of nickel(II) oxide nanoparticles on lymphocytes of human peripheral blood

Dumala

Mangalampalli

Grover

2019

J of Applied Toxicology

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The current study was intended to elucidate the cytotoxicity, genotoxicity ability of nickel oxide (NiO) nanoparticles (NPs) and assessment of preliminary mechanism of the toxicity. Characterization studies showed that NiO‐NPs have a particle size of 17.94 (±3.48) nm. The particle size of the NPs obtained by dynamic light scattering method in Milli‐Q and RPMI 1640 media was 189.9 (±17.1) and 285.9 (±19.6) nm, respectively. The IC50 concentration for NiO‐NPs after 24 hours of treatment was estimated as 23.58 μg/mL. Comet and cytokinesis‐block micronucleus assays revealed a significant dose‐ and time‐dependent genotoxic potential of NiO‐NPs. Morphological assessment of the lymphocytes upon exposure to NiO‐NPs showed that the mechanism of toxicity was apoptosis. Reactive oxygen species analysis and lipid peroxidation patterns were aligned with the cytotoxicity and genotoxicity endpoints. Thus, the preliminary mechanism of NiO‐NPs for cytotoxicity on lymphocytes was assumed to be oxidative stress‐mediated apoptosis and DNA damage. Furthermore, these NiO‐NPs are considered a potentially hazardous substance at environmentally significant levels. Further investigations are suggested to understand the immunotoxic effects of NiO‐NPs.

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“…Despite its wide application, Nano NiO is also known for its harmful effects and draws increasing attention to health science researchers. Nano NiO causes reactive oxygen species (ROS) generation, oxidative stress, DNA damage, apoptosis, and transcriptome alterations in HepG2 cells . In addition, chronic liver damage promotes hepatic fibrosis in animal models .…”

Section: Introductionmentioning

confidence: 99%

TGF‐β1 mediated Smad signaling pathway and EMT in hepatic fibrosis induced by Nano NiO in vivo and in vitro

Zhang

Chang

Wang

et al. 2019

Environmental Toxicology

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Nickel oxide nanoparticles (Nano NiO) bears hepatotoxicity, while whether it leads to liver fibrosis remains unclear. The aim of this study was to establish the Nano NiO‐induced hepatic fibrosis model in vivo and investigate the roles of transforming growth factor β1 (TGF‐β1) in Smad pathway activation, epithelial‐mesenchymal transition (EMT) occurrence, and extracellular matrix (ECM) deposition in vitro. Male Wistar rats were exposed to 0.015, 0.06, and 0.24 mg/kg Nano NiO by intratracheal instilling twice a week for 9 weeks. HepG2 cells were treated with 100 μg/mL Nano NiO and TGF‐β1 inhibitor (SB431542) to explore the mechanism of collagen formation. Results of Masson staining as well as the elevated levels of type I collagen (Col‐I) and Col‐III suggested that Nano NiO resulted in hepatic fibrosis in rats. Furthermore, Nano NiO increased the protein expression of TGF‐β1, p‐Smad2, p‐Smad3, alpha‐smooth muscle actin (α‐SMA), matrix metalloproteinase9 (MMP9), and tissue inhibitors of metalloproteinase1 (TIMP1), while decreased the protein content of E‐cadherin and Smad7 in rat liver and HepG2 cells. Most importantly, Nano NiO‐triggered the abnormal expression of the abovementioned proteins were all alleviated by co‐treatment with SB431542, implying that TGF‐β1‐mediated Smad pathway, EMT and MMP9/TIMP1 imbalance were involved in overproduction of collagen in HepG2 cells. In conclusion, these findings indicated that Nano NiO induced hepatic fibrosis via TGF‐β1‐mediated Smad pathway activation, EMT occurrence, and ECM deposition.

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Nickel Oxide Nanoparticles Induced Transcriptomic Alterations in HEPG2 Cells

Cited by 31 publications

References 46 publications

Intestinal Epithelial Cell Toxicity Induced By Nickel Oxide Nanoparticles

Intestinal Epithelial Cell Toxicity Induced By Nickel Oxide Nanoparticles

Retracted: In vitro genotoxicity assessment of nickel(II) oxide nanoparticles on lymphocytes of human peripheral blood

TGF‐β1 mediated Smad signaling pathway and EMT in hepatic fibrosis induced by Nano NiO in vivo and in vitro

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