A study of the mechanism of in vitro cytotoxicity of metal oxide nanoparticles using catfish primary hepatocytes and human HepG2 cells

Wang, Yonggang; Aker, Winfred G.; Hwang, Huey‐Min; Yedjou, Clément G.; Yu, Hongtao; Tchounwou, Paul B.

doi:10.1016/j.scitotenv.2011.07.039

Cited by 160 publications

(92 citation statements)

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“…50 ZnO NPs (47-106 nm) induced cytotoxicity and ROS generation in HepG2 human hepatocellular carcinoma cells. 51 ZnO NPs (uncoated 100 nm and triethoxycaprylylsilane-coated 130 nm) were 50% soluble, which could account for their cytotoxicity. 52 Moreover, both ZnO NPs (but not other NPs tested) decreased albumin production by C3A human hepatoblastoma cells, suggesting effects on hepatic function.…”

Section: In Vitro Studies Using Other Cell Linesmentioning

confidence: 99%

A review of mammalian toxicity of ZnO nanoparticles

Vandebriel¹,

Jong²

2012

NSA

442

247

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This review summarizes the literature on mammalian toxicity of ZnO nanoparticles (NPs) published between 2009 and 2011. The toxic effects of ZnO NPs are due to the compound's solubility. Whether the increased intracellular [Zn 2+ ] is due to the NPs being taken up by cells or to NP dissolution in medium is still unclear. In vivo airway exposure poses an important hazard. Inhalation or instillation of the NPs results in lung inflammation and systemic toxicity. Reactive oxygen species (ROS) generation likely plays an important role in the inflammatory response. The NPs do not, or only to a minimal extent, cross the skin; this also holds for sunburned skin. Intraperitoneal administration induces neurological effects. The NPs show systemic distribution; target organs are liver, spleen, lung, and kidney and, in some cases, the heart. In vitro exposure of BEAS-2B bronchial epithelial cells and A549 alveolar adenocarcinoma cells results in cytotoxicity, increased oxidative stress, increased intracellular [Ca 2+ ], decreased mitochondrial membrane potential, and interleukin (IL)-8 production. Decreased contractility of airway smooth muscle cells poses an additional hazard. In contrast to the results for BEAS-2B and A549 cells, in RKO colon carcinoma cells ZnO NPs and not Zn 2+ induce cytotoxicity and mitochondrial dysfunction. Short-term exposure of skin cells results in apoptosis but not in an inflammatory response, while long-term exposure leads to increased ROS generation, decreased mitochondrial activity, and formation of tubular intercellular structures. Macrophages, monocytes, and dendritic cells are affected; exposure results in cytotoxicity, oxidative stress, intracellular Ca 2+ flux, decreased mitochondrial membrane potential, and production of IL-1β and chemokine CXCL9. The NPs are phagocytosed by macrophages and dissolved in lysosomes. In vitro the Comet assay and the cytokinesis-blocked micronucleus assay show genotoxicity, whereas the Ames test does not. This is, however, not confirmed by in vivo genotoxicity assays. Protein binding results in increased stability.

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Section: In Vitro Studies Using Other Cell Linesmentioning

confidence: 99%

A review of mammalian toxicity of ZnO nanoparticles

Vandebriel¹,

Jong²

2012

NSA

442

247

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“…Recent studies reported nanoparticle-induced oxidative stress as determined by increasing membrane lipid peroxidation (LPO) and reactive oxygen species (ROS) levels and decreasing intracellular reduced glutathione (GSH) level. 9 We evaluated the oxidative stress biomarkers, including GSH levels; ROS generation as a collective marker of superoxide anion, hydroxyl radical, and hydrogen peroxide levels; as well as LPO, in response to Al 2 O 3 NP exposure.…”

Section: Introductionmentioning

confidence: 99%

Nanoalumina induces apoptosis by impairing antioxidant enzyme systems in human hepatocarcinoma cells

Alarifi¹,

Ali²,

Alkahtani³

2015

IJN

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Alumina nanoparticles (Al 2 O 3 NPs) are gradually used in various areas, including nanomedicine, biosensors, and electronics. The current study aimed to explore the DNA damage and cytotoxicity due to Al 2 O 3 NPs on human hepatocarcinoma cells (HepG2). The MTT and neutral red uptake assays showed that Al 2 O 3 NPs induce significant cell death in a dose- and time-dependent manner. However, Al 2 O 3 NPs induced significant intracellular reactive oxygen species production and elevated lipid peroxidation and superoxide dismutase levels in the HepG2 cells. Al 2 O 3 NPs also induced significant decrease in reduced glutathione levels and increase caspase-3 activity in HepG2 cells. DNA fragmentation analysis using the alkaline single-cell gel electrophoresis showed that Al 2 O 3 NPs cause genotoxicity in dose- and time-dependent manner. However, they induce reactive oxygen species production and oxidative stress, leading to oxidative DNA damage, a probable mechanism of genotoxicity. This study warrants more careful assessment of Al 2 O 3 NPs before their industrial application.

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“…It has been reported that different sizes and morphologies of NPs have the potential to influence the interaction with many kind of biomolecules, including proteins, enzymes and DNA (Grandjean-Laquerriere et al 2005;Ramesh et al 2007;Xu et al 2012). The liver was considered as a target site for nanotoxicity due to its accumulative properties after ingestion, inhalation or absorption (Wang et al 2011). However, recorded hepatotoxicity data for WO 3 NPs relating to human health are very scarce.…”

Section: Introductionmentioning

confidence: 99%