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Interaction of Microspheres and Nanoparticles with Cells and Tissues

The behaviour of nanoand microplastics after they have entered the circulation from the gut is not fully understood, but has been the subject of study in relation to food packaging materials and nanomedicines. Certainly, in vivo behaviour will be dependent on numerous factors, such as the physico-chemical properties of the particles (size, surface charge, aspect ratio, porosity, surface corona) and the physiological state of the individual. Risk assessments of manufactured nanomaterials including titanium dioxide (Wang et al. 2007) and carbon (Poland et al. 2008) have shown comparable results to those shown above for nanopolymers, with uptake across the gut into the circulation and redistribution to the liver and spleen. Circulation time is highly dependent on the surface characteristics of the particle, with hydrophilic and positively charged particles showing enhanced circulation times (Silvestre et al. 2011).

Interactions with Biological Materials and Cells

Interaction of nanopolymers with cells and tissues has again been the subject of intensive study. Because of their surface properties, nanopolymers are predicted to adsorb macromolecules such as proteins and lipids from the surrounding body fluids onto their surface, in a process influenced by surface energy, charge and specific affinity for certain biomolecules. The resulting 'corona' will then influence the resulting behaviour and toxicity of the particle (Lundqvist et al. 2008; Tenzer et al. 2013). This process has been extensively studied for polymers intended for therapeutic use particularly using polystyrene as a model polymer, but little or nothing is known of how protein coronas may form on the types of polymers most commonly found in environmental debris.

The results from mechanistic studies of different types of particle show that the potential for cytotoxicity of circulating particles in vivo to cells and tissues is related to many factors, including size, shape, solubility, surface charge, surface reactivity and energy band structure (Nel et al. 2006; Burello and Worth 2011). For example, it would be reasonable to hypothesize that particles with a high abundance of reactive surface groups would be capable of denaturing surrounding lipids and proteins. As an illustration of this, the toxicity of silica nanoparticles in vivo was attributed to proton donating silanol groups on the surface of the particles, leading to denaturation of membrane proteins and subsequent membrane damage. In this case, the reactivity of the surface hydrogen of silica bonds with membrane proteins led to their abstraction from the membrane, with subsequent membrane damage and distortion leading to haemolytic symptoms following exposure (Pandurangi et al. 1990).

Surface charge is also a strong attributing factor for toxicity (Geys et al. 2008). In inhalation studies in rats, the toxicity of acrylic ester nanopolymers in the size range 50–1500 nm was found to be low, and this was attributed to their anionic surface charge (Ma-Hock et al. 2012). Studies in which the surface charge of stearylamine-polylactic acid (PLA) polymers was modified from positive to negative showed that cationic particles showed higher pulmonary toxicity (HarushFrenkel et al. 2010). This was attributed both to a higher localisation of cationic particles in the lung and to enhanced cellular uptake. Overall, the interaction of cationic polymers with the negatively charged cell surface has been proposed as a cause of their higher cytotoxicity (Fischer et al. 2003).

Translocation of nanopolymers into diverse tissues and cell types presents another point at which toxicity may occur. Translocation is dependent on interactions with the cell membrane and is most likely to proceed, as for uptake by enterocytes in the gut, through pinocytic, phagocytic and receptor-mediated endocytosis (Fruijter-Polloth 2012). A study, which measured the uptake rates of individual polystyrene microspheres into human astrocytes and lung carcinoma cells in culture found that the uptake rate differed for particles of different sizes, implying that there are differences in the mechanisms involved. Particles with a diameter of 40 nm showed higher uptake rates than either 20 or 100 nm particles. Since the van der Waals force between a sphere and a surface is proportional to the diameter of the sphere (Israelachvili 1992), it could be predicted that larger particles would be taken up faster. The conclusion was that the endocytic mechanism for internalisation of 40 nm particles exhibited faster kinetics, providing a privileged size gap for 40 nm particles (Varela et al. 2012).

Phagosomes containing particles may fuse with endosomes following internalisation, leading to accumulation of particles in lysosomes. Depending on the dose and type of particle, this has the potential to overwhelm lysosomal capacity and interfere with programmed cell death and pathways of cellular breakdown of pathogens (Fruijter-Polloth 2012). The numerous additional modes of toxicity that may result are again dependent on particle and cell type, and include the potential for oxidative damage, inflammation and accumulation in diverse tissue types (Silvestre et al. 2011; Nel et al. 2006, 2009). In theory, all organs may be at risk following chronic exposure to nanopolymers, including the brain, testis and reproductive organs, prior to their eventual excretion in urine and faeces (Jani et al. 1996; Garrett et al. 2012). Distribution to the foetus in utero is also a possibility that cannot be excluded. Given the long-term persistence of many polymer types, more research is required to adequately assess the risks that accumulation of microand nanoplastics in the body may pose.

 
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