In vitro toxicity of iron oxide nanoparticle: Oxidative damages on Hep G2 cells

Sadeghi, Leila; Tanwir, Farzeen; Babadi, Vahid Yousefi

doi:10.1016/j.etp.2014.11.010

Cited by 53 publications

(39 citation statements)

References 27 publications

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“…Comparison of different assays shows the correlation between intracellular ROS level and toxic effects on cells. Moreover, it was also demonstrated that Fe 2 O 3 nanoparticles induce oxidative stress followed by significant modifications of different protein expression, leading to Hep G2 cells apoptosis in a time‐dependent manner . These facts confirm that induced by IONP ROS formation serves as one of the main reasons for such materials cytotoxicity.…”

Section: Discussionmentioning

confidence: 53%

Toxicity of iron oxide nanoparticles: Size and coating effects

Abakumov

Semkina

Skorikov

et al. 2018

J Biochem & Molecular Tox

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Toxicological research of novel nanomaterials is a major developmental step of their clinical approval. Since iron oxide magnetic nanoparticles have a great potential in cancer treatment and diagnostics, the investigation of their toxic properties is very topical. In this paper we synthesized bovine serum albumin‐coated iron oxide nanoparticles with different sizes and their polyethylene glycol derivative. To prove high biocompatibility of obtained nanoparticles the number of in vitro toxicological tests on human fibroblasts and U251 glioblastoma cells was performed. It was shown that albumin nanoparticles’ coating provides a stable and biocompatible shell and prevents cytotoxicity of magnetite core. On long exposure times (48 hours), cytotoxicity of iron oxide nanoparticles takes place due to free radical production, but this toxic effect may be neutralized by using polyethylene glycol modification.

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Section: Discussionmentioning

confidence: 53%

Toxicity of iron oxide nanoparticles: Size and coating effects

Abakumov

Semkina

Skorikov

et al. 2018

J Biochem & Molecular Tox

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“…Significant reductions of cellular levels of glutathione peroxidase and superoxide dismutase levels as well as increased MDA were also observed. Sadeghi and coworkers [35] analyzed the effects of Fe 3 O 4 -NP exposures (75–100 µg/mL) in HepG2 cells after 12–24 h of treatment. Higher oxidative damage to DNA that was both concentration and time dependent was detected.…”

Section: Discussionmentioning

confidence: 99%

Magnetic Hyperthermia and Oxidative Damage to DNA of Human Hepatocarcinoma Cells

Cellai

Munnia

Viti

et al. 2017

IJMS

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Nanotechnology is addressing major urgent needs for cancer treatment. We conducted a study to compare the frequency of 3-(2-deoxy-β-d-erythro-pentafuranosyl)pyrimido[1,2-α]purin-10(3H)-one deoxyguanosine (M1dG) and 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG) adducts, biomarkers of oxidative stress and/or lipid peroxidation, on human hepatocarcinoma HepG2 cells exposed to increasing levels of Fe3O4-nanoparticles (NPs) versus untreated cells at different lengths of incubations, and in the presence of increasing exposures to an alternating magnetic field (AMF) of 186 kHz using 32P-postlabeling. The levels of oxidative damage tended to increase significantly after ≥24 h of incubations compared to controls. The oxidative DNA damage tended to reach a steady-state after treatment with 60 μg/mL of Fe3O4-NPs. Significant dose–response relationships were observed. A greater adduct production was observed after magnetic hyperthermia, with the highest amounts of oxidative lesions after 40 min exposure to AMF. The effects of magnetic hyperthermia were significantly increased with exposure and incubation times. Most important, the levels of oxidative lesions in AMF exposed NP treated cells were up to 20-fold greater relative to those observed in nonexposed NP treated cells. Generation of oxidative lesions may be a mechanism by which magnetic hyperthermia induces cancer cell death.

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“…Human hepatoma-derived Hep G2 cells (obtained from National Center for Cell Sciences, Pasteur Institute of Iran, Tehran) were seeded in RPMI-1640 media supplemented with 2 mg/ml sodium bicarbonate, 10% (v/v) fetal bovine serum, 100 unit/ml penicillin, and 100 mg/ml streptomycin at 37°C and 5% CO 2 incubator. [15] Cells reached to the approximately 60% confluence during 24 h and then were treated with 100 µg/ml CPF, 100 µg/ml PILO or 50 µg/ml CPF + 50 µg/ml PILO (CPF + PILO) during 48 h. We tried to use doses of drugs that have less cytotoxic effects on Hep G2 cells; therefore, dose of CPF and PILO was determined based on previous studies. [8,16] Cells free of drugs (CPF and PILO) were used as control group in each experiment.…”

Section: Cell Culture and Experimental Designmentioning

confidence: 99%

“…Cell viability was evaluated by using MTT assay, which was based on the conversion of the MTT dye to formazan crystals, an insoluble intracellular blue crystal, by cellular dehydrogenases. [15] A total of 5 9 10 5 cells were incubated in 96-well plate with 50 µl medium per well. The cells were cultured in the medium containing 100 µg/ml of CPF and/ or PILO for 48 h after 2 h stabilizing.…”

Section: Cell Viability Assaymentioning

confidence: 99%

“…The intracellular concentrations of ROS were determined by measuring the oxidation of DCFH-DA to dichlorofluorescin (DCFH), as a fluorescent compound. [15] Briefly, Hep G2 were cultured in 24-well plates for 12 h, treated with CPF and/or PILO, incubated with DCF diacetate in culture medium for 15 min and washed with cold phosphate buffer solution three times. Resulted green fluorescence (from oxidized DCFH) was assessed using a microplate fluorimeter (LB 941; Berthold Technologies, Bad Wildbad, Germany) with excitation at 488 nm and emission at 530 nm.…”

Section: Reactive Oxygen Species (Ros) Measurementmentioning

confidence: 99%

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Cumulative effects of ciprofloxacin and pilocarpine on cytotoxicity and G0 phase arrest in hepatoma-derived Hep G2 cell line

Sadeghi

Maleki

Dehghan

2020

Journal of Pharmacy and Pharmacology

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Objectives Uncontrolled cell proliferation was caused by multiple deficient pathways that inhibition of one pathway may result to activate an alternative pathway. Therefore, combination of drugs which targeted multiple pathways could be beneficial to overcome drug resistance. Ciprofloxacin (CPF) cytotoxicity was widely investigated on cancer cell lines, and results revealed hepatoma‐derived Hep G2 cells are relatively resistant. So, this study aimed to increase CPF cytotoxicity by rational design of a supplement which targeted Ca2+ homoeostasis as major hub in unchecked proliferation. Methods Cells were treated by CPF and/or pilocarpine (PILO), and cell cycle distribution, caspases activity and regulatory proteins were evaluated. Key findings MTT and flow cytometry analysis confirmed administration of CPF + PILO causes more cytotoxicity. CPF‐exposed cells accumulated in S phase due to DNA damages while PILO + CPF imposed G0 stage arrest through cyclin D1 and P‐Akt downregulation. Caspase 8 was activated in cells treated by CPF but accompaniment of PILO with CPF led to activation of caspase 9, 8 and 3 and ROS overproduction. Conclusions Ciprofloxacin imposed mitochondrial‐independent apoptosis while PILO + CPF caused mitochondrial‐dependent and independent apoptosis simultaneously. Consequently, coadministration of PILO and CPF causes intense cytotoxic effects through targeting the mitochondria, DNA gyrase enzyme and other unknown mechanisms.

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In vitro toxicity of iron oxide nanoparticle: Oxidative damages on Hep G2 cells

Cited by 53 publications

References 27 publications

Toxicity of iron oxide nanoparticles: Size and coating effects

Toxicity of iron oxide nanoparticles: Size and coating effects

Magnetic Hyperthermia and Oxidative Damage to DNA of Human Hepatocarcinoma Cells

Cumulative effects of ciprofloxacin and pilocarpine on cytotoxicity and G0 phase arrest in hepatoma-derived Hep G2 cell line

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