Ecotoxicology of Manufactured Nanoparticles - Environmental and Human Health Impacts of Nanotechnology - page 279

To date, the generation of ROS is the most discussed and best developed
model for nanoparticle toxicity and has primarily developed from studies with
ultrafi ne particles (UFPs) in human health toxicology (Chapter 9). Reactive oxygen
species may react with cells via a number of mechanisms and if present at suffi -
ciently high concentrations will lead to oxidative stress. Intracellularly an excess of
ROS may cause damage to DNA, proteins and organelles. Mitochondria are con-
sidered to be an intracellular target for nanoparticle deposition (Li et al. , 2003 ;
Oberdorster et al. , 2005) and mitochondrion can themselves be a source of free
electrons leaking from the electron transport chain (Unfried et al. , 2007 ). This may
potentiate the effects of redox active nanoparticles leading to further production
of O 2 or other free radical species (Nel et al. , 2006 ; Unfried et al. , 2007 ). In pro-
karyotes, the electron transport chain is located in the cell envelope, thus a similar
mechanism may contribute to bacterial membrane damage. In human cell lines,
the cytotoxicity of water soluble fullerene species has been shown to be mediated
via reactive oxygen species causing lipid peroxidation and membrane damage
(Sayes et al. , 2004, 2005). However, other studies have shown that soluble n C 60
species may act as antioxidants and protect against radical initiated lipid peroxida-
tion (Wang et al. , 1999 ; Nel et al. , 2006 ).
A number of ecotoxicological investigations have considered oxidative stress as
a mechanism for nanoparticle toxicity. Rainbow trout ( Oncorhynchus mykiss )
exposed to nanoparticulate titanium dioxide showed an increase in oxidative stress
markers in the gill, intestine and brain (Federici et al. , 2007) and water solubilised
n C 60 elevated lipid peroxidation in the brain and gill tissue of adult fathead minnow
( Pimephales promelas ) (Zhu et al. , 2006). However, none of these studies directly
measured ROS generation in the experimental media, so it is unclear if oxidative
stress was a due to ROS generation directly from the nanoparticles or was a result
of an immunological response. Adams et al. (2006a, 2006b) showed that illumina-
tion (direct sunlight, 6 h) increased the antibacterial activity of TiO 2 and SiO 2 to E.
coli and B. subtilis , supporting the view that the toxicity of these metal oxides is
related to ROS production. However, there was no effect of pre-illumination (250
watts, 30 min) on the toxicity of TiO 2 to the green alga Desmodesmus subspicatus ,
suggesting ROS generation was not a major mechanism of toxicity (Hunde-Rinke
and Simon, 2006).

7.3.4 Bioaccumulation

The uptake and gradual accumulation of nanoparticles by living organisms may
lead to cumulative toxicity effects. These effects may of course be counteracted by
the organism's ability to detoxify accumulated particles either by excretion, pas-
sivation or storage in a benign form. It is also conceivable that the trophic transfer
of bioaccumulated nanoparticles may occur. Nanoparticles also have the potential
to accumulate (or adsorb) other toxins in the environment, such as heavy metals
or persistent organics, and to facilitate their transport into living organisms, thus
enhancing their bioavailability and/or bioaccumulation. Titanium dioxide nanopar-
ticles have been demonstrated to enhance the bioaccumulation of heavy metals
such as arsenic and cadmium in freshwater fi sh (Sun et al. , 2007 ; Zhang et al. , 2007 ).