Ecotoxicology of Manufactured Nanoparticles - Environmental and Human Health Impacts of Nanotechnology - page 276

mechanisms in eukaryotes. However, nanoparticles may also be taken into the
tissues of aquatic organisms by ingestion or across the gill surface epithelia. Roberts
et al. (2007) showed that water fl eas ( Daphnia magna ) rapidly ingested lipid-coated
nanotubes via normal feeding behaviour (Figure 7.8b), metabolising the lipid
coating as a food source. In fi sh, single-walled carbon nanotubes (SWCNTs) have
been observed in the gut lumen of animals exposed to sub-lethal (0.1 mg/l) concen-
trations for 10 days, which was associated with an increase in oxidative stress
markers and ionoregulatory disturbance (Smith et al. , 2007 ).

7.3.3 Toxicity Mechanisms

Nanoparticles may cause cellular toxicity via a number of different mechanisms
including, but not limited to, physical damage, dissolution of toxic ions or species
and generation of reactive oxygen species (Figure 7.7). As discussed in the preced-
ing section, the large surface area and abrasive nature of some nanoparticles may
be suffi cient to infl ict suffi cient non - specifi c physical damage to cell membranes
and/or organelles to cause toxicity or cell death.

7.3.3.1 Membrane Damage

Nanoparticulate materials may elicit an acute toxic response either directly at the
cell membrane or by gaining uptake into the cell. Nanocrystals can be prepared
with very high surface areas and possess crystal morphologies with numerous
edges, corners, defects and other reactive sites (Klabunde et al. , 1996 ; Stoimenov
et al. , 2002). The abrasive nature of such particles may bestow the potential to infl ict
non - specifi c physical damage to cell membranes. Stoimenov et al. (2002) reported
that halogenated adducts of magnesium oxide nanoparticles induced major damage
to bacterial cell membranes resulting in leakage of the cell contents and cell death
(Figure 7.9). Both silver (Morones et al. , 2005) and zinc oxide (Brayner et al. , 2006 )
nanoparticles have also been shown damage to bacterial membranes when exposed
in the high mg/l range.
Kang et al. (2007) exposed Escherichia coli cells to pristine SWCNTs (5 mg/l)
with a narrow diameter distribution (0.75-1.2 nm) and demonstrated that direct
contact between bacterial cells and the SWCNTs caused severe membrane damage
and subsequent cell inactivation. Membrane damage may be an especially impor-
tant toxicity mechanism for unicellular organisms with limited capacity to recover
from massive physical damage to the cell envelope; however, microbes can also
serve as useful models in elucidating cytotoxicity mechanisms that can be extrapo-
lated to eukaryotic cells (Wiesner et al. , 2006). Damage to the membranes of human
cell lines has been demonstrated for nano-C 60 colloidal suspensions (Sayes et al. ,
2005). Given the outcomes of these studies, membrane damage should be consid-
ered as a possible mechanism of nanoparticle toxicity in ecotoxicological studies
on eukaryotes and also a potentially signifi cant process for both aquatic and
terrestrial bacteria that come into contact with nanoparticles.
Histopathological evidence indicates that the membranes of fi sh gills are damaged
by exposure SWCNTs (Smith et al. , 2007 ), nano - TiO 2 (Federici et al. , 2007 ) and