Consecutive evaluation of graphene oxide and reduced graphene oxide nanoplatelets immunotoxicity on monocytes

Yan, Junyan; Chen, Liliang; Huang, Chih‐Ching; Lung, Shih-Chun Candice; Yang, Lingyan; Wang, Wencheng; Lin, Po-Hsiung; Suo, Guangli; Lin, Chia‐Hua

doi:10.1016/j.colsurfb.2017.02.036

Cited by 42 publications

(29 citation statements)

References 46 publications

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“…We initially measured the extent of cytotoxicity caused by GO to RAW264.7 cells. Effective cell death was observed upon the treatment of 0.1‐10 μg/mL GO for 24 hours (Supporting Information Figure S6), which were also observed in THP‐1 cells . Following the mRNA levels of TNFα and IL‐8 in RAW264.7 cells after 24 hours GO exposure was then examined.…”

Section: Resultsmentioning

confidence: 93%

Developmental neurotoxicity and immunotoxicity induced by graphene oxide in zebrafish embryos

Yang

Zheng

et al. 2018

Environmental Toxicology

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Graphene oxide (GO) has emerged as the worldwide promising candidate for biomedical application, such as for drug delivery, bio-sensing and anti-cancer therapy. This study was focused on the zebrafish and RAW264.7 cell line as in vivo and in vitro models to assess the potential developmental neurotoxicity and immunotoxicity of GO. No obvious acute developmental toxicity was observed upon treatments with 0.01, 0.1, and 1 μg/mL GO for five consecutive days.However, decreased hatching rate, increased malformation rate, heart beat rate and hypoactivity of locomotor behavior were detected when exposed to 10 μg/mL GO. Also, RT-PCR analysis revealed that expressions of genes related to the nervous system were up-regulated. The potential risk of GO for developmental neurotoxicity may be ascribed to the high level of oxidative stress induced by high concentration of GO. Most importantly, the mRNA levels of immune response associated genes, such as interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNFα), interferon-γ (IFN-γ) were significantly increased under environmental concentration exposure. The activation of pro-inflammatory immune response was also observed in macrophage cell line. Taken together, our results demonstrated that immunotoxicity is a sensitive indicator for assessment of bio-compatibility of GO. K E Y W O R D S embryotoxicity, graphene oxide, oxidative stress, Raw264.7 cells, zebrafish

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Section: Resultsmentioning

confidence: 93%

Developmental neurotoxicity and immunotoxicity induced by graphene oxide in zebrafish embryos

Yang

Zheng

et al. 2018

Environmental Toxicology

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“…46 FLG was also shown to exert a selective killer action towards monocytes. 47,48 Similarly, pro-inflammatory effects of GBNs were also observed on macrophages, with GO being able to activate the inflammasome 49 and enhance the production of inflammatory cytokines 50 in a size-dependent manner. Altogether, these observations support the hypothesis of proinflammatory properties of GBNs at the cutaneous level.…”

Section: Discussionmentioning

confidence: 95%

Graphene and graphene oxide induce ROS production in human HaCaT skin keratinocytes: the role of xanthine oxidase and NADH dehydrogenase

et al. 2018

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The extraordinary physicochemical properties of graphene-based nanomaterials (GBNs) make them promising tools in nanotechnology and biomedicine. Considering the skin contact as one of the most feasible exposure routes to GBNs, the mechanism of toxicity of two GBNs (few-layer-graphene, FLG, and graphene oxide, GO) towards human HaCaT skin keratinocytes was investigated. Both materials induced a significant mitochondrial membrane depolarization: 72 h cell exposure to 100 μg mL-1 FLG or GO increased mitochondrial depolarization by 44% and 56%, respectively, while the positive control valinomycin (0.1 μg mL-1) increased mitochondrial depolarization by 48%. Since the effect was not prevented by cyclosporine-A, it appears to be unrelated to mitochondrial transition pore opening. By contrast, it seems to be mediated by reactive oxygen species (ROS) production: FLG and GO induced time- and concentration-dependent cellular ROS production, significant already at the concentration of 0.4 μg mL-1 after 24 h exposure. Among a panel of specific inhibitors of the major ROS-producing enzymes, diphenyliodonium, rotenone and allopurinol significantly reverted or even abolished FLG- or GO-induced ROS production. Intriguingly, the same inhibitors also significantly reduced FLG- or GO-induced mitochondrial depolarization and cytotoxicity. This study shows that FLG and GO induce a cytotoxic effect due to a sustained mitochondrial depolarization. This seems to be mediated by a significant cellular ROS production, caused by the activation of flavoprotein-based oxidative enzymes, such as NADH dehydrogenase and xanthine oxidase.

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“…Moreover, several in vitro studies showed significant effects of GBMs on immune cells. [49][50][51][52][53][54] Thus, in vivo studies should be carried out to elucidate the effects of GBMs on the immune system, also considering the use of these materials as biomedical tools.…”

Section: Nanoscale Reviewmentioning

confidence: 99%

Occupational exposure to graphene based nanomaterials: risk assessment

et al. 2018

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Graphene-based materials (GBMs) are a family of novel materials including graphene, few layer graphene (FLG), graphene oxide (GO), reduced graphene oxide (rGO) and graphene nanoplatelets (GNP). Currently, the risk posed by them to human health is associated mainly with the occupational exposure during their industrial and small-scale production or waste discharge. The most significant occupational exposure routes are inhalation, oral, cutaneous and ocular, inhalation being the majorly involved and most studied one. This manuscript presents a critical up-to-date review of the available in vivo toxicity data of the most significant GBMs, after using these exposure routes. The few in vivo inhalation toxicity studies (limited to 5-days of repeated exposure and only one to 5 days per week for 4 weeks) indicate inflammatory/fibrotic effects at the pulmonary level, not always reversible after 14/90 days. More limited in vivo data are available for the oral and ocular exposure routes, whereas the studies on cutaneous toxicity are at the initial stage. A long persistence of GBMs in rodents is recorded, while contradictory genotoxic data are reported. Data gap identification is also provided. Based on the available data, the occupational exposure limit cannot be determined. More experimental toxicity studies according to specific guidelines (tentatively validated for nanomaterials) and more information on the actual occupational exposure level to GBMs are needed. Furthermore, ADME (Absorption, Distribution, Metabolism, Excretion), genotoxicity, developmental and reproductive toxicity data related to the occupational exposure to GBMs have to be implemented. In addition, sub-chronic and/or chronic studies are still needed to completely exclude other toxic effects and/or carcinogenicity.

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Consecutive evaluation of graphene oxide and reduced graphene oxide nanoplatelets immunotoxicity on monocytes

Cited by 42 publications

References 46 publications

Developmental neurotoxicity and immunotoxicity induced by graphene oxide in zebrafish embryos

Developmental neurotoxicity and immunotoxicity induced by graphene oxide in zebrafish embryos

Graphene and graphene oxide induce ROS production in human HaCaT skin keratinocytes: the role of xanthine oxidase and NADH dehydrogenase

Occupational exposure to graphene based nanomaterials: risk assessment

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