High-throughput transcriptomics: An insight on the pathways affected in HepG2 cells exposed to nickel oxide nanoparticles

Saquib, Quaiser; Xia, Pu; Siddiqui, Maqsood A.; Zhang, Junjiang; Xie, Yuwei; Faisal, Mohammad; Ansari, Sabiha M.; Alwathnani, Hend A.; Alatar, Abdulrahman A.; Al‐Khedhairy, Abdulaziz A.; Zhang, Xiaowei

doi:10.1016/j.chemosphere.2019.125488

Cited by 21 publications

(15 citation statements)

References 46 publications

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“…Cell cycle in HUVECs exposed to carbofuran was analyzed by following the previously described method (Saquib et al, 2020). HUVECs (1 × 10 6 cells/well) were exposed to carbofuran (10, 25, 50, 100, 250, 500, and 1,000 μM) for 24 h in an incubator at 37°C (CO 2 5% and 95% humidity).…”

Section: Methodsmentioning

confidence: 99%

Carbofuran cytotoxicity, DNA damage, oxidative stress, and cell death in human umbilical vein endothelial cells: Evidence of vascular toxicity

Saquib

Siddiqui

Ansari

et al. 2021

J of Applied Toxicology

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Carbofuran is a broad‐spectrum carbamate insecticide, which principally inhibits the acetylcholinesterase (AChE) enzyme in the nervous system. Nonetheless, their selective action is not restricted to a single species and expanded to humans. No studies are available on the toxicological effects of carbofuran in the endothelial cells (ECs), which first confronts the toxicants in blood vessels. Hence, we have exposed the human umbilical vein ECs (HUVECs) with carbofuran for 24 h, which significantly reduced the cell survival to 25.16% and 33.48% at 500 and 1,000 μM analyzed by MTT assay. In the neutral red uptake (NRU) assay, 16.68%, 30.99%, and 58.11% survival decline was found at 250, 500, and 1,000 μM of carbofuran. HUVECs exposed to carbofuran showed significant increase in the intracellular reactive oxygen species (ROS), indicating oxidative stress at low concentrations. In parallel, HUVECs showed hyperpolarization effects in the mitochondrial membrane potential (ΔΨm) upon carbofuran exposure. Carbofuran induced DNA damage in HUVECs measured as 8.80, 11.82, 35.56, and 79.69 Olive tail moment (OTM) in 100‐, 250‐, 500‐, and 1,000‐μM exposure groups. Flow cytometric analysis showed apoptotic peak (SubG1) and G2M arrest in the HUVECs exposed to carbofuran. Overall, our novel data confirm that carbofuran is toxic for the EC cells, especially at the higher concentrations, which may affect the vascular functions and possibly angiogenesis. Hence, carbofuran should be applied judiciously, and detailed vascular studies are warranted to gain an in‐depth information focusing the transcriptomic and translation changes employing suitable in vivo and in vitro test models.

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Section: Methodsmentioning

confidence: 99%

Carbofuran cytotoxicity, DNA damage, oxidative stress, and cell death in human umbilical vein endothelial cells: Evidence of vascular toxicity

Saquib

Siddiqui

Ansari

et al. 2021

J of Applied Toxicology

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“…HUVECs were analyzed on a flow cytometer (Coulter Epics XL/XL‐MCL, Miami, USA) for changes in cell cycle (Saquib et al, 2020). In brief, HUVECs were grown in the presence of 5, 10, 25, 50, 100, 200, and 400 μM of TCPP for 24 h in a CO 2 incubator (5%, 37°C).…”

Section: Methodsmentioning

confidence: 99%

Organophosphorus flame‐retardant tris(1‐chloro‐2‐propyl)phosphate is genotoxic and apoptotic inducer in human umbilical vein endothelial cells

Saquib

Siddiqui

Al‐Khedhairy

2021

J of Applied Toxicology

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Tris(1‐chloro‐2‐propyl)phosphate (TCPP) is a chlorinated organophosphorus flame retardant (OPFR) widely used in consumer goods after the phaseout of brominated flame retardants (BFRs). TCPP can percolate into the indoor and outdoor dusts, leading to its detection in the human body fluids (urine, breast milk) and placenta. However, TCPP has not been studied so far for its toxicity in the human vascular system. Hence, we have used human umbilical vein endothelial cells (HUVECs) and exposed them to TCPP ranging from low to high (5–400 μM) concentrations for 24 h. Cytotoxicity analysis by MTT and NRU assays exhibited 15.27% and 20.56%, 21.67%, and 48.67% survival decline of cells only at 200 and 400 μM. Comet assay data showed DNA damage from 50 to 400 μM with Olive tail moment (OTM) values between 1.03 and 35.59, respectively. TCPP‐exposed HUVECs exhibited 1.09 and 1.39‐fold greater intracellular reactive oxygen species (ROS) at 25 and 400 μM, indicating oxidative stress. HUVEC mitochondrial membrane potential (ΔΨm) measurements showed 1.16 and 1.48‐fold higher fluorescence of Rh123 dye at 25 and 400 μM, confirming mitochondrial dysfunction. Flow cytometric data demonstrated 5.1%–58.8% cells in SubG1 apoptotic phase at 5 and 400 μM TCPP. Our novel data revealed that TCPP is a genotoxic and apoptotic inducer, which may trigger alike responses in human vascular system. Overall, detailed in vivo studies are warranted on the transcriptional and translations effects of TCPP.

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“…There was also stronger expression of superoxide dismutase (SOD) as well as p53, Bax and Bcl2 [37]. Transcriptional analysis using total RNA-sequencing revealed [38] that changes in expression of HepG2 cells genes occurred when NiO NPs concentrations exceeded 5 µg/ml. Expression of hypoxia-related HIF-1 and micro-RNA(miR)-210 grew under exposure to 25-100 µg/ml of these NPs; and there were variable changes in trascriptome including activations of glycolysis metabolic pathways, glutathione synthesis, lysosome digestion and autophagy even under exposure to concentrations that didn't cause any apparent cytotoxic effects.…”

Section: Cytotoxicity Of Ni-containing Nanomaterialsmentioning

confidence: 99%

Assessing risks caused by nickel-based nanomaterials: hazardous factor identification

Gmoshinski¹,

lane²,

Хотимченко³

2021

Health Risk Analysis

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Nanoparticles of nickel (Ni) and its compounds attract a lot of attention bearing in mind their promising innovative properties allowing their use as catalysts, components in electrical appliances, electronic devices and photonic appliances, and materials used in producing medications, diagnostic preparations, and pesticides. Production volumes of these materials in their nano-form are likely to grow rapidly in the nearest future and it involves greater loads created by these nanomaterials on a human body. And we should remember that Ni and its compounds are highly toxic for humans even in their traditional disperse forms. Their toxicity induces oxidative stress, cellular membranes and mitochondria dysfunction, expression of nuclear transcription factors that are responsible for apoptosis, caspases, as well as proto-oncogenes. Leading role in toxicity of Ni-containing nanomaterials obviously belongs to ions of heavy Ni++ being emitted from them since this heavy metal has pro-oxidant properties and influences enzyme activity and gene expression. Cytotoxic effects produced by Ni-containing nanomaterials were revealed in Model experiments in vitro performed with suing cellular cultures that were morphologically and functionally similar to epithelial cells of respiratory and gastrointestinal tract, liver, kidneys, and nervous system; these materials were able to stimulate oxidant stress, influence expression of apoptosis proteins and nuclear transcription factors, induce apoptosis and necrosis. There are data indicating that Ni-containing nanomaterials can produce malignant transforming effects in vitro. All the above mentioned proves that nickel compounds in their nanoform are a new hazardous factor that requires assessing related risks for workers, consumer, and population in general. Our review focuses on analyzing literature sources on cytotoxicity of Ni-containing nanomaterials and their effects produced on molecular-genetic and cellular levels taken over a period starting from 2011.

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High-throughput transcriptomics: An insight on the pathways affected in HepG2 cells exposed to nickel oxide nanoparticles

Cited by 21 publications

References 46 publications

Carbofuran cytotoxicity, DNA damage, oxidative stress, and cell death in human umbilical vein endothelial cells: Evidence of vascular toxicity

Carbofuran cytotoxicity, DNA damage, oxidative stress, and cell death in human umbilical vein endothelial cells: Evidence of vascular toxicity

Organophosphorus flame‐retardant tris(1‐chloro‐2‐propyl)phosphate is genotoxic and apoptotic inducer in human umbilical vein endothelial cells

Assessing risks caused by nickel-based nanomaterials: hazardous factor identification

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