Table 2.
Nanoparticle-membrane interaction.
Nanomaterial class | Nanomaterial | Cell lines/ lipid membranes | Material properties | Biological effect | Interactions/Mediated pathway | Year | Ref. |
---|---|---|---|---|---|---|---|
Carbon based | C60(OH)20 | Allium cepa cells | Concentration: 10–110 mg L−1 Solubility: water soluble Size: (1–24 nm) Surface charge: −43 mV |
Plant cell wall permeation, Plasma membrane exclusion, cell damage | Hydrophilicity, electrostatic repulsion, H-bonding, Van der Waals | ||
HT-29 cells | Low affinity for cell membrane | ||||||
C70–NOM | Allium cepa cells | Concentration: 10–110 mg L−1
Solubility: hydrophobic and clustered in high concentrations (10–100 nm) Surface charge: −34 mV |
Plant cell wall protection | Hydrophobic interactions, non-covalent assembly | 2010 | [105] | |
HT-29 cells | Cell lysis | ||||||
S/L-SWNTs | Size (diameter): (1–3 nm) Size (length): S-SWNTs (50–100 nm) |
Cell nucleus localization | Nuclear envelope transport, energy independent pathway, clathrin-dependent endocytosis, caveolae-dependent endocytosis | 2010 | [106] | ||
Hep G2 cells | Size (diameter): (1–3 nm) Size (length): L-SWNTs (100–200 nm) |
Cytoplasm localization | Clathrin-dependent endocytosis | ||||
S/L-MWNTs | Size (diameter): (10–30 nm) Size (length): S-MWNTs (0.5–1 μm) Size (diameter): (10–30 nm) Size (length): L-MWNTs (1–2 μm) |
FA receptor mediated endocytosis | Receptor binding | ||||
GQDs | MDCK monolayer cells | Size: 3 nm, 12 nm Surface charge: −1 mV (3 nm), −15 mV (12 nm) |
Time, concentration (~300 mg L−1) and size dependent cell membrane permeability. Noninduced cell lysis and plasma membrane penetration | Lipid raft-mediated transcytosis | 2015 | [107] | |
GO-OH/COOH | POPC/POEPC, POPC/POPS (3:1) liposomes | Surface charge: 22 mV (POPC/POEPC (3:1) liposomes), −26 mV (POPC/POPS (3:1) liposomes), −56 mV (GO, pH 4) | Rupture of pre-adsorbed positively charged liposomes (QCM-D frequency shift), multilayered structure formation | Electrostatic interactions, H-bonding | 2012 | [108] | |
GO (pristine/oxidized) | A549 and Raw264.7 cells | Layer: Single (thickness ~1 nm) Size: (200–700 nm) Raman bands: D (~1350 cm−1) and G (~1598 cm−1) Oxidization degree: 26.1% |
Cell death and pore hole formation (non- autophagy) induced at concentrations 50 to 200 μg/mL. | Phospholipid extraction on GO surface (unstable Stage I) (↓Van der Waals energy), balance between internal membrane tension and graphene-mediated dispersion force (metastable Stage II), membrane tension, lipid extraction and pore formation (↓ Van der Waals energy) (stable Stage III) | 2017 | [109] | |
DOPC lipid bilayer sandwiched GO | J774A (macrophage) and 4T1 (breast cancer) cells | Size: ~40 nm (GO) Height: Less than 2 nm Layer: Single or double |
Transport inside of cell membrane (Lévy and directional dynamics), pore hole formation | 2019 | [110] | ||
S/L-GO sheets | Primary human neutrophils | Layer: Single or double (thickness: 1–2 nm) Size: GO-S (50–300 nm), GO-L (10–40 μm) Surface charge: −55 mV, −37 mV in cell culture medium |
Dose-dependent loss of cell viability, membrane stripping, size-dependent (GO-L) NET induced production (Ca+2, ROS dependent), elevation of oxidized cholesterol species | Potential interaction with positively charged histones (NET), lipid oxidation | 2018 | [111] | |
Metal based | TiO2NPs | HMVEC monolayer and MDA-MB-231 cells | Size: 57 nm (in cell culture medium) Surface charge: −24 mV (in cell culture medium) | Dose (10–1250 μM) and size (nanoscale) dependent endothelial cell leakiness (NanoEL) due to cell junction (VE-cadherin) disruption, further promoting breast cancer cell intravasation | Electrostatic interactions between negatively charged TiO2 NPs and positively charged VE-cadherin side chains. Homophilic loss of cell-cell interaction | 2013, 2019 | [112– 113] |
AuNPs | HMVEC, HMMEC and HUVEC monolayer | Size: 10–30 nm Surface charge: ~−8 mV (in cell culture medium) SPR peak: 518 nm (Au10), 523 nm (Au30) |
NanoEL | Disruption of VE-cadherin-VE-cadherin interactions | 2017 | [114] | |
MSNs (MCM-41 and SBA-15) | RBC membranes | Size: ~600 nm (SBA-15), ~100 nm (MCM-41) | Size- (larger-> higher hemolytic activity) and surface (large surface->larger binding energy)- dependent interaction and engulfment between MSN and RBC membranes | Binding of silanol-rich surface of MSNs with phosphatidyl choline-rich RBC membrane | 2011 | [115] | |
Surface modified (Au based) | AuNPs | CP70, ASM, A2780, BEC cells | Plasma membrane charge: between −75 and −55 mV Size: 2 nm (AuNP core) |
Surface charge (+AuNPs) → rapid plasma membrane depolarization, intracellular uptake and [Ca2+]i elevation. Concentration dependant (0–1.2 mM) | Electrostatic interactions | 2010 | [116] |
PVA-AuNPs | A549 and J774A.1 cells | Surface charge: Range of −3 mV to −14 mV in cell culture medium Functional groups: Primary, secondary, tertiary amino groups | Increased NP-cell membrane association for primary amines with high amine density (A549) combined with high protein adsorption (serum albumin, alpha-2-HS-glycoprotein) irrespective of amine density | Salt bridge formation, hydrophobicity, conformational effect on PVA coating and accessibility toward polar amino acids of serum proteins | 2018 | [117] | |
Ligand-AuNPs | POPC, DOPC/DOPS (−), DOPC/DOEPC (+) A549 cells | Size: 13 nm Surface ligands: MW, charge, and bonding categorization, small molecules, biomacromolecules |
Ligand’s size and adsorption affinity-two main factors for ligand exchange with lipid molecules Influence on endocytic pathways, uptake efficiency, cell membrane integrity |
Electrostatic, hydrophobic and Van der Waals interactions | 2019 | [118] | |
Ligand-coated AuNRs | SOPC monolayer, THP-1 cells | Diameter, length: CTAB/PDC-AuNRs (~15, ~60 nm) Surface charge: CTAB/PDC-AuNRs (30–40 mV in H2O, −13 mV in serum and H2O) Ligand-NR stability: (PDC>CTAB) |
Weaker ligand stability and further detachment lead to membrane thickness decrease (SOPC), lysosomal membrane penetration, concentration dependent cytotoxicity and inflammation | CTAB-AuNRs (Van der Waals), PDCAuNRs (Hydrophobic and electrostatic interactions). CTAB-AuNRs-SOPC (↓Van der Waals, electrostatic interactions) | 2019 | [119] | |
Protein corona | BSA-PMASH NPPs | THP-1 monocytic and dTHP-1 macrophage cells | Surface charge: −25 mV in BSA medium | Reduced cellular association and internalization by protein-NPP complexes than NPPs in monocyte cells. Differential cellular association in dTHP-1 cells (SR-A-mediated phagocytosis) | Structural conformation of BSA upon protein corona formation influences binding with SR-A | 2013 | [121] |
BSA/HSA/HDL-AgNPs | RLE and RAEC cells | Size: 19 nm (AgNPs), 70 nm (HSA-AgNPs), 31 nm (BSA-AgNPs), 62 nm (HDL-AgNPs) Surface charge: −35 mV (AgNPs), −25 mV (HSA-AgNPs), −18 mV (BSA-AgNPs), −8 mV (HDL-AgNPs) |
Reduced cytotoxicity of protein corona AgNPs in both cells lines at high concentrations (50 μg/ml) at 3 h and 6 h. Increased inflammatory response for HDL-AgNPs in RLE cells IL-6 mRNA expression: AgNPs (control, RLE, RAEC cells), HSA-AgNPs (↓-RLE, RAEC cells) BSA-AgNPs (↓-RLE, RAEC cells), HDL-AgNPs (↑-RLE cells, ↓-RAEC cells), Samples in the presence of Blt2 inhibitor (↓-RLE, RAEC cells) |
Cell surface receptor-mediated signaling. Intracellular Ag+ release. Loss of protein corona upon internalization | 2014 | [122] | |
HSA (modified)- DHLA-QDs | HeLa cells | HSA modified species: succinylated HSA (HSAsuc), aminated HSA (HSAam) Surface charge: −11 mV (HSA-QDs), −19 mV (HSAsuc-QDs), −6 mV (HSAam-QDs) |
Enhanced membrane binding and cell internalization of HSAsuc-coated-QDs and respective suppression by HSAam-coated-QDs due to modified charge distributions | Active pinocytic (clathrin-mediated) pathway to endosomes and lysosomes | 2014 | [123] | |
Deglycosylated protein corona SiO2NPs | dTHP-1 (M1, M2 macrophages) cells | Size: 126–139 nm Surface charge: ~9 mV |
Enhanced cell membrane adhesion, nanoparticle uptake and stimulation of pro-inflammatory responses | Influence of glycosylation on immune activation | 2015 | [124] | |
Hard/soft corona (human serum) PS-NPs (PS, PS-COOH, PS-NH2 | Raw264.7 cells | Size (NP soft corona): 140 nm (PS), 178 nm (PS-COOH), 188 nm (PS-NH2) Size (NP hard corona):92 nm (PS), 80 nm (PS-COOH), 88 nm (PS-NH2) Hard corona thickness: 15 nm Surface charge: −4 mV (PS), −1 (PS-COOH), 1 mV (PS-NH2) |
Differential cellular uptake between soft corona or Apo-A1 PS-NPs (inhibition) and hard corona PS-NPs. Significant enhanced uptake for hard corona PS-COOH-NPs | CLIC/GEEC endocytosis pathway for bare PS-NPs. Similar structural properties (large corona diameter ~100 nm and large number of Apo-A1 proteins) for soft corona and Apo-A1 PS-NPs lead to uptake inhibition | 2017 | [125] |