Effects of graphene oxide nanosheets on the ultrastructure and biophysical properties of the pulmonary surfactant film

Hu, Qingxi; Jiao, Bao Xiang; Shi, Xinghua; Valle, Russell P.; Zuo, Yi Y.; Hu, Guoqing

doi:10.1039/c5nr05401j

Cited by 56 publications

(66 citation statements)

References 44 publications

(61 reference statements)

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“…16,26 Consequently, the hydrophobic NPs are expected to have a higher inhibitory potential to the biophysical function of natural PS than the hydrophilic NPs. Along this line, our in vitro experiments showed that NPs with increasing hydrophobicity cause a higher degree of surfactant inhibition, likely due to depletion of hydrophobic proteins from the natural PS.…”

Section: Resultsmentioning

confidence: 99%

Unveiling the Molecular Structure of Pulmonary Surfactant Corona on Nanoparticles

et al. 2017

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The growing risk of human exposure to airborne nanoparticles (NPs) causes a general concern on the biosafety of nanotechnology. Inhaled NPs can deposit in the deep lung at which they interact with the pulmonary surfactant (PS). Despite the increasing study of nano-bio interactions, detailed molecular mechanisms by which inhaled NPs interact with the natural PS system remain unclear. Using coarse-grained molecular dynamics simulation, we studied the interaction between NPs and the PS system in the alveolar fluid. It was found that regardless of different physicochemical properties, upon contacting the PS, both silver and polystyrene NPs are immediately coated with a biomolecular corona that consists of both lipids and proteins. Structure and molecular conformation of the PS corona depend on the hydrophobicity of the pristine NPs. Quantitative analysis revealed that lipid composition of the corona formed on different NPs is relatively conserved and is similar to that of the bulk phase PS. However, relative abundance of the surfactant-associated proteins, SP-A, SP-B, and SP-C, is notably affected by the hydrophobicity of the NP. The PS corona provides the NPs with a physicochemical barrier against the environment, equalizes the hydrophobicity of the pristine NPs, and may enhance biorecognition of the NPs. These modifications in physicochemical properties may play a crucial role in affecting the biological identity of the NPs and hence alter their subsequent interactions with cells and other biological entities. Our results suggest that all studies of inhalation nanotoxicology or NP-based pulmonary drug delivery should consider the influence of the PS corona.

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Section: Resultsmentioning

confidence: 99%

Unveiling the Molecular Structure of Pulmonary Surfactant Corona on Nanoparticles

et al. 2017

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“…When GO was inhaled into the human body through the blood-air barrier, it was able to destroy the biophysical properties and ultrastructure of pulmonary surfactant film, resulting in potential toxicity (Hu et al, 2015). When GO was inhaled into the human body through the blood-air barrier, it was able to destroy the biophysical properties and ultrastructure of pulmonary surfactant film, resulting in potential toxicity (Hu et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Dose‐dependent cytotoxicity induced by pristine graphene oxide nanosheets for potential bone tissue regeneration

Zhang

Wei

et al. 2019

J Biomedical Materials Res

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This study was aimed to investigate the toxic effects of pristine graphene oxide (GO) nanosheets on bone-marrow-derived mesenchymal stem cells (BMSCs), a type of traditional seed cells in tissue regeneration engineering. First, a GO suspension was prepared and characterized by transmission electron microscopy, Fourier transform infrared spectroscopy, and Raman shifts. Then, rat BMSCs were isolated and characterized. Subsequently, cell proliferation, membrane integrity, cell cycle, cell apoptosis, mitochondrial membrane potential (MMP), and reactive oxygen species (ROS) were measured. In addition, relevant proteins of the mitochondrial apoptotic pathway and autophagy were analyzed. Our results showed that a high concentration of GO inhibited cell viability and membrane integrity, while cell apoptosis and cellcycle arrest were induced by GO. Further, GO significantly increased ROS generation and MMP loss with an upregulation of Cleaved Caspase-3, LC3-II/I, and Beclin-1 and a downregulation of Bcl-2 and Caspase3. We concluded that the toxic effects of GO on BMSCs occurred in a dose-dependent manner via the mitochondrial apoptotic pathway and autophagy.

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“…The inhaled GO nanosheets can destroy the ultrastructure and biophysical properties of pulmonary surfactant (PS) film, which is the first line of host defense, and emerge their potential toxicity [54]. The agglomerated or dispersed particles deposit on the inner alveolar surface within the alveoli and then be engulfed by alveolar macrophages (AMs) [55].…”

Section: Toxicity Of Gfns (In Vivo and In Vitro)mentioning

confidence: 99%

Toxicity of graphene-family nanoparticles: a general review of the origins and mechanisms

et al. 2016

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Due to their unique physicochemical properties, graphene-family nanomaterials (GFNs) are widely used in many fields, especially in biomedical applications. Currently, many studies have investigated the biocompatibility and toxicity of GFNs in vivo and in intro. Generally, GFNs may exert different degrees of toxicity in animals or cell models by following with different administration routes and penetrating through physiological barriers, subsequently being distributed in tissues or located in cells, eventually being excreted out of the bodies. This review collects studies on the toxic effects of GFNs in several organs and cell models. We also point out that various factors determine the toxicity of GFNs including the lateral size, surface structure, functionalization, charge, impurities, aggregations, and corona effect ect. In addition, several typical mechanisms underlying GFN toxicity have been revealed, for instance, physical destruction, oxidative stress, DNA damage, inflammatory response, apoptosis, autophagy, and necrosis. In these mechanisms, (toll-like receptors-) TLR-, transforming growth factor β- (TGF-β-) and tumor necrosis factor-alpha (TNF-α) dependent-pathways are involved in the signalling pathway network, and oxidative stress plays a crucial role in these pathways. In this review, we summarize the available information on regulating factors and the mechanisms of GFNs toxicity, and propose some challenges and suggestions for further investigations of GFNs, with the aim of completing the toxicology mechanisms, and providing suggestions to improve the biological safety of GFNs and facilitate their wide application.

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Effects of graphene oxide nanosheets on the ultrastructure and biophysical properties of the pulmonary surfactant film

Cited by 56 publications

References 44 publications

Unveiling the Molecular Structure of Pulmonary Surfactant Corona on Nanoparticles

Unveiling the Molecular Structure of Pulmonary Surfactant Corona on Nanoparticles

Dose‐dependent cytotoxicity induced by pristine graphene oxide nanosheets for potential bone tissue regeneration

Toxicity of graphene-family nanoparticles: a general review of the origins and mechanisms

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