Skip to main content
. Author manuscript; available in PMC: 2021 Oct 1.
Published in final edited form as: Adv Nanobiomed Res. 2020 Nov 26;1(1):2000040. doi: 10.1002/anbr.202000040

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 [112113]
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]