Magnetic iron oxide nanoparticles induce autophagy preceding apoptosis through mitochondrial damage and ER stress in RAW264.7 cells

Park, Eun Jung; Choi, Dong Hyuk; Kim, Younghun; Lee, Eun Woo; Song, Jaewhan; Cho, Myung‐Haing; Kim, Jae Ho; Kim, Sang Wook

doi:10.1016/j.tiv.2014.07.010

Cited by 98 publications

(50 citation statements)

References 60 publications

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“…9 Furthermore, IONPs may induce cytokine production in various immune cells. For example, γ-Fe 2 O 3 nanoparticles can increase TNF in RAW264.7 cells 10 and carboxydextran-coated Fe 3 O 4 /Fe 2 O 3 nanoparticles induced TNF in THP-1 cells. 11 Moreover, non-coated and polyacrylic acid-coated IONPs induced IL-1β, IL-8, IL-6, TNF and IL-10 in primary human blood cells 12 and aminopolyvinyl alcohol-coated SPION increased the secretion of IL-1β, IL-4, IL-8, IL-6, MIP-1β and RANTES in whole blood samples.…”

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confidence: 99%

Iron oxide nanoparticles induce cytokine secretion in a complement-dependent manner in a human whole blood model

Wolf-Grosse¹,

Rokstad²,

Ali³

et al. 2017

IJN

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Iron oxide nanoparticles (IONPs) are promising nanomaterials for biomedical applications. However, their inflammatory potential has not been fully established. Here, we used a lepirudin anti-coagulated human whole blood model to evaluate the potential of 10 nm IONPs to activate the complement system and induce cytokine production. Reactive oxygen species and cell death were also assessed. The IONPs activated complement, as measured by C3a, C5a and sC5b-9, and induced the production of pro-inflammatory cytokines in a particle-dose dependent manner, with the strongest response at 10 µg/mL IONPs. Complement inhibitors at C3 (compstatin analog Cp40) and C5 (eculizumab) levels completely inhibited complement activation and secretion of inflammatory mediators induced by the IONPs. Additionally, blockade of complement receptors C3aR and C5aR1 significantly reduced the levels of various cytokines, indicating that the particle-induced secretion of inflammatory mediators is mainly C5a and C3a mediated. The IONPs did not induce cell death or reactive oxygen species, which further suggests that complement activation alone was responsible for most of the particle-induced cytokines. These data suggest that the lepirudin anti-coagulated human whole blood model is a valuable ex vivo system to study the inflammatory potential of IONPs. We conclude that IONPs induce complement-mediated cytokine secretion in human whole blood.

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confidence: 99%

Iron oxide nanoparticles induce cytokine secretion in a complement-dependent manner in a human whole blood model

Wolf-Grosse¹,

Rokstad²,

Ali³

et al. 2017

IJN

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“…AgNPs induced autophagic flux defect may consequently lead to aggravated cytotoxic responses [38]. Park's results showed us that M FeNPs induce autophagy preceding apoptosis through mitochondrial dysfunction and ER stress in RAW 264.7 cells [39]. The mechanism is similar to carbon nano as we said above.…”

Section: Autophagy and Nanomaterialsmentioning

confidence: 64%

The Role of Cell Autophagy in Toxicity Caused by Dental Nanomaterials

Wei¹

2017

NTMB

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NanomaterialsThe overview of nanomaterials Nanomaterials are defined as materials composed of unbound particles or particles in an aggregate or agglomerate state with one or more external dimensions with a size ranging from 1nm to 100nm [1]. Nanomaterials have a lot of free surfaces and interfaces and there is interaction between the various units. Based on the above characteristics, nanomaterials are featured by surface effect, small size effect, quantum size effect, macroscopic quantum tunneling effect and the dielectric confinement effect. Nanoparticles have lots of unpaired atoms, large specific surface area, less surface defects and can occur in conjunction with the polymer stronger physically or chemically. Added to the polymer material, they can improve the ductility, toughness, strength, barrier properties, heat resistance and dimensional stability of the material. They have been widely used in conventional materials, medical equipment, electronic equipment, paint and other industries. However, nanomaterials will affect the organism and produce a series of toxic effects by inducing oxidative stress and inflammatory response mechanisms in the cell, subcellular and protein levels. The nanomaterials commonly used in dentistryNanometer materials are widely applied in the field of dentistry, including dental restoration, antibacterial, caries treatment, orthodontic, root canal, bonding systems and so on.Adding nanoparticles to dental restoration materials to improve the performance has been widely used in the clinical field. In view of its unpaired atoms, large specific surface area, less surface defects and occurring in conjunction with the polymer either stronger physically or chemically, the novel resin composite exhibited a strong antibacterial property upon the addition of up to 5% nano antibacterial inorganic fillers, there by leading to effective caries inhibition in dental application [2]. The mesoporous silica biomaterials have great potential for serving as both a catalyst and carrier in the repair or regeneration of dental hard tissue [3]. Diatomite-based nanocomposite ceramics are good potential candidates for ceramic-based dental materials [4]. Nano silicon dioxide can also give polymers the characteristics of better viscosity, thermal stability, high strength, less volume shrinkage and of course, durability [5].In clinical endodontics especially root canal and restorative treatments we can see the near future potential of nanoparticles from the application of nanoparticles in the form of solutions for irrigation, medication and as an additive within sealers/restorative materials [6]. GICs can be applied to base plates of Orthodontic and modified denture base well, as which contain chlorhexidine hexametaphosphate nanoparticles and characterize the nanoparticle size shows a stronger antimicrobial activity [7].As for caries treatment, Hannig M said that Analysis of in vitro data indicates that apatite nanoparticles might be effective in reversing lesion progression in the outer but not in the deepe...

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“…The generation of oxidative DNA lesions, such as those caused from Fe 3 O 4 -NPs [45], has intensified interest in nanotoxicology because they are considered one way to induce of authophagy and apoptosis cell death of cancer cells [46]. When DNA is severely damaged or unrepaired, cells may remain quiescent and activate pro-survival mechanisms or undergo cell death.…”

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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Magnetic iron oxide nanoparticles induce autophagy preceding apoptosis through mitochondrial damage and ER stress in RAW264.7 cells

Cited by 98 publications

References 60 publications

Iron oxide nanoparticles induce cytokine secretion in a complement-dependent manner in a human whole blood model

Iron oxide nanoparticles induce cytokine secretion in a complement-dependent manner in a human whole blood model

The Role of Cell Autophagy in Toxicity Caused by Dental Nanomaterials

Magnetic Hyperthermia and Oxidative Damage to DNA of Human Hepatocarcinoma Cells

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