% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Heikkil:154397,
      author       = {Heikkilä, Elena and Martinez-Seara, Hector and Gurtovenko,
                      Andrey A. and Javanainen, Matti and Häkkinen, Hannu and
                      Vattulainen, Ilpo and Akola, Jaakko},
      title        = {{C}ationic {A}u {N}anoparticle {B}inding with {P}lasma
                      {M}embrane-like {L}ipid {B}ilayers: {P}otential {M}echanism
                      for {S}pontaneous {P}ermeation to {C}ells {R}evealed by
                      {A}tomistic {S}imulations},
      journal      = {The journal of physical chemistry / C},
      volume       = {118},
      number       = {20},
      issn         = {1932-7455},
      address      = {Washington, DC},
      publisher    = {Soc.},
      reportid     = {FZJ-2014-03744},
      pages        = {11131 - 11141},
      year         = {2014},
      abstract     = {Despite being chemically inert as a bulk material,
                      nanoscale gold can pose harmful side effects to living
                      organisms. In particular, cationic Au nanoparticles (AuNP+)
                      of 2 nm diameter or less permeate readily through plasma
                      membranes and induce cell death. We report atomistic
                      simulations of cationic Au nanoparticles interacting with
                      realistic membranes and explicit solvent using a model
                      system that comprises two cellular compartments,
                      extracellular and cytosolic, divided by two asymmetric lipid
                      bilayers. The membrane–AuNP+ binding and membrane
                      reorganization processes are discovered to be governed by
                      co-operative effects where AuNP+, counterions, water, and
                      the two membrane leaflets all contribute. On the
                      extracellular side, we find that the nanoparticle has to
                      cross a free energy barrier of about 5 kBT prior forming a
                      stable contact with the membrane. This results in a
                      rearrangement of the zwitterionic lipids and nanoparticle
                      side groups in the contact area, giving rise to the initial
                      stage of pore formation on the membrane surface. Such
                      behavior is not seen on the cytosolic side, where AuNP+ is
                      spontaneously captured by the negatively charged
                      phosphatidylserine lipids that diffuse to enrich the
                      membrane leaflet underneath AuNP+, further pointing to AuNP+
                      accumulation on the inner leaflet of a plasma membrane. The
                      results suggest AuNP+ permeation to take place through the
                      formation of a pore together with partial nanoparticle
                      neutralization/deprotonation, leading to membrane disruption
                      at higher nanoparticle concentrations. The data also suggest
                      a potential mechanism for cytotoxicity as AuNP+ binding to
                      the extracellular leaflet may trigger apoptosis through
                      translocation of phosphatidylserine.},
      cin          = {PGI-1},
      ddc          = {540},
      cid          = {I:(DE-Juel1)PGI-1-20110106},
      pnm          = {422 - Spin-based and quantum information (POF2-422)},
      pid          = {G:(DE-HGF)POF2-422},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000336509400068},
      doi          = {10.1021/jp5024026},
      url          = {https://juser.fz-juelich.de/record/154397},
}