Ultrafine Particles Cross Cellular Membranes by Nonphagocytic Mechanisms in Lungs and in Cultured Cells
By M. Geiser, B. Rothen‐Rutishauser, N. Kapp, S. Schürch, W. Kreyling, H. Schulz, M. Semmler, V. Hof, J. Heyder, P. Gehr. Environmental Health Perspectives, 2005
1,351 citations recorded by the source corpus.
High concentrations of airborne particles have been associated with increased pulmonary and cardiovascular mortality, with indications of a specific toxicologic role for ultrafine particles (UFPs; particles < 0.1 μm). Within hours after the respiratory system is exposed to UFPs, the UFPs may appear in many compartments of the body, including the liver, heart, and nervous system. To date, the mechanisms by which UFPs penetrate boundary membranes and the distribution of UFPs within tissue compartments of their primary and secondary target organs are largely unknown. We combined different experimental approaches to study the distribution of UFPs in lungs and their uptake by cells. In the in vivo experiments, rats inhaled an ultrafine titanium dioxide aerosol of 22 nm count median diameter. The intrapulmonary distribution of particles was analyzed 1 hr or 24 hr after the end of exposure, using energy-filtering transmission electron microscopy for elemental microanalysis of individual particles. In an in vitro study, we exposed pulmonary macrophages and red blood cells to fluorescent polystyrene microspheres (1, 0.2, and 0.078 μm) and assessed particle uptake by confocal laser scanning microscopy. Inhaled ultrafine titanium dioxide particles were found on the luminal side of airways and alveoli, in all major lung tissue compartments and cells, and within capillaries. Particle uptake in vitro into cells did not occur by any of the expected endocytic processes, but rather by diffusion or adhesive interactions. Particles within cells are not membrane bound and hence have direct access to intracellular proteins, organelles, and DNA, which may greatly enhance their toxic potential.
Subfields: Environmental Engineering, Health, Toxicology and Mutagenesis, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/36b3c89e4c3f2348b52fc5412f6409b5ef80f88e
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In Environmental Engineering
In Health, Toxicology and Mutagenesis
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Citations in the corpus
- Toxicology of nanoparticles: A historical perspective (2007, neutral): “Diffusion may be a likely mechanism of uptake of these very small particles into cells (Figure 6E) as suggested by Geiser et al. (2005).”
- Traffic Related Air Pollution, Particulate Matter, and Autism (2013, neutral): “1) may penetrate cellular membranes.(37,38) These particles translocate indirectly through the lungs and from the systemic circulation or directly via the nasal mucosa and the olfactory bulb into the brain.”
- NanoGenotoxicology: the DNA damaging potential of engineered nanomaterials. (2009, background): “Indeed, it has been shown that nanoparticles of titanium dioxide and silica can enter the nucleus [17,18] where they cause intranuclear protein aggregates that can lead to inhibition of replication, transcription, and cell proliferation [19].”
- Long-term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the Blood-Brain Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid β-42 and α-Synuclein in Children and Young Adults (2008, background): “…ECs and RBCs could represent a pathway for the exchange of PM between the activated endothelial cell and the UFPM-loaded RBCs, in keeping with the capacity of ultrafine PM to penetrate RBC, as elegantly shown by Geiser and Rothen-Rutishauser (Geiser et al. 2005; Rothen-Rutishauser et al. 2006).”
- The Adverse Effects of Air Pollution on the Nervous System (2012, background): “These mechanisms may include electrostatic, van der Waals, and steric interactions and are subsumed under the term adhesive interaction, although the exact mechanisms remain to be determined [13, 33].”
- Airborne microplastics: Consequences to human health? (2018, positive): “Polystyrene has been shown to internalize efficiently in various cultured cell lines (Zauner et al., 2001), including rat alveolar epithelial cells (Yacobi et al., 2008), erythrocytes (Geiser et al., 2005) and macrophages (Geiser et al., 2005; Kruth et al., 1999).”
- Nanodiamond Particles: Properties and Perspectives for Bioapplications (2009, background): “403 Other non-specific uptake mechanisms including pinocytosis, patocytosis, or membrane ruffling may unsuspectingly traffic nanomaterials into cells.”
- Better safe than sorry: Understanding the toxicological properties of inorganic nanoparticles manufactured for biomedical applications. (2010, background): “[134] reported that uptake of fluorescent polystyrene beads (78 nm) in vitro by porcine lung macrophages occurs through a passive (nonphagocytic) mechanism.”