2017; Römer et al. 2013). In the case of CNPs, the chemical transformations such as
Ce(IV) to Ce(III) cycling and associated soluble species are likely to be vital for
understanding their biological and environmental behaviors (Graham et al. 2014; Li
et al. 2012; Lópezmoreno et al. 2010; Thill et al. 2006). In particular, the redox
reactions between CNPs and redox-active ions or (in)organic ligands will strongly
impact their surface properties and consequently their transport, reactivity, and
toxicity in terrestrial and aquatic environments (Barton et al. 2014; Liu et al. 2015;
Rollin-Genetet et al. 2015; Safi et al. 2010). Furthermore, transformations mediated
by microorganisms and exposure media may alter the core of CNPs and their surface
functional groups, leading to altered surface composition, agglomeration state, and
toxicity potential (Barton et al. 2014; Dowding et al. 2013; Louie et al. 2014; Römer
et al. 2013). Therefore, it is necessary to systematically shed light on the distribution,
transformation and speciation of CNPs under different environmental exposure
conditions as well as the related ecosystem impacts.
Since mounting growth of commercial CNPs production will result in potentially
negative influences on ecosystems, the underlying mechanisms are urgently
required. In several reports on the toxicity of CNPs (Fang et al. 2010; Heckert
et al. 2008; Kuang et al. 2011; Pešić et al. 2015), the biological impact of CNPs
has been investigated at the cellular and molecular levels. At the cellular level, CNPs
were generally considered to be a prooxidant, resulting in the induction of oxidative
stress and cytotoxicity after cell internalization (Ma et al. 2016; Park et al. 2008b;
Pešić et al. 2015). At the molecular level, when CNPs enter the cytoplasm, they tend
to interact with biological components like protein and nucleates, which lead to key
enzyme inactivation and DNA damage (Collin et al. 2014; Liu et al. 2013; Marie
et al. 2014; Milani et al. 2012). Furthermore, considering the chemical process, the
redox property of ceria with transition between Ce(III) and Ce(IV) is of critical
importance to understand its potential toxicity mechanisms, for the transformation
between Ce(IV) and Ce(III) makes CNPs acting as quenchers or producers of
reactive oxygen species (ROS) (Thill et al. 2006; Zhang et al. 2011). Nevertheless,
the intrinsic physicochemical properties and further transformations of CNPs in the
exposure systems are ignored in drawing the general conclusions and perspectives
for the potential mechanisms on CNPs toxicity.
Accordingly, the aims of this review are to (1) highlight and discuss types of
physicochemical properties relating to the bioaccumulation and toxicity of CNPs;
(2) illustrate the distribution, translocation, and speciation of CNPs under different
environmental scenarios, with an emphasis on the bioaccumulation and toxicity
outcomes; (3) discuss the phase transformation of CNPs core during interacting
with environmental components as well as the results of such transformations on
toxicity; and (4) underline the potential physiological and biochemical impacts of
CNPs and propose the related mechanisms. Finally, important knowledge gaps that
need to be addressed to better understand the potential risk, safe production, and
handling of CNPs are raised.
Surface Properties and Environmental Transformations Controlling the. . .
159
Ce(IV) to Ce(III) cycling and associated soluble species are likely to be vital for
understanding their biological and environmental behaviors (Graham et al. 2014; Li
et al. 2012; Lópezmoreno et al. 2010; Thill et al. 2006). In particular, the redox
reactions between CNPs and redox-active ions or (in)organic ligands will strongly
impact their surface properties and consequently their transport, reactivity, and
toxicity in terrestrial and aquatic environments (Barton et al. 2014; Liu et al. 2015;
Rollin-Genetet et al. 2015; Safi et al. 2010). Furthermore, transformations mediated
by microorganisms and exposure media may alter the core of CNPs and their surface
functional groups, leading to altered surface composition, agglomeration state, and
toxicity potential (Barton et al. 2014; Dowding et al. 2013; Louie et al. 2014; Römer
et al. 2013). Therefore, it is necessary to systematically shed light on the distribution,
transformation and speciation of CNPs under different environmental exposure
conditions as well as the related ecosystem impacts.
Since mounting growth of commercial CNPs production will result in potentially
negative influences on ecosystems, the underlying mechanisms are urgently
required. In several reports on the toxicity of CNPs (Fang et al. 2010; Heckert
et al. 2008; Kuang et al. 2011; Pešić et al. 2015), the biological impact of CNPs
has been investigated at the cellular and molecular levels. At the cellular level, CNPs
were generally considered to be a prooxidant, resulting in the induction of oxidative
stress and cytotoxicity after cell internalization (Ma et al. 2016; Park et al. 2008b;
Pešić et al. 2015). At the molecular level, when CNPs enter the cytoplasm, they tend
to interact with biological components like protein and nucleates, which lead to key
enzyme inactivation and DNA damage (Collin et al. 2014; Liu et al. 2013; Marie
et al. 2014; Milani et al. 2012). Furthermore, considering the chemical process, the
redox property of ceria with transition between Ce(III) and Ce(IV) is of critical
importance to understand its potential toxicity mechanisms, for the transformation
between Ce(IV) and Ce(III) makes CNPs acting as quenchers or producers of
reactive oxygen species (ROS) (Thill et al. 2006; Zhang et al. 2011). Nevertheless,
the intrinsic physicochemical properties and further transformations of CNPs in the
exposure systems are ignored in drawing the general conclusions and perspectives
for the potential mechanisms on CNPs toxicity.
Accordingly, the aims of this review are to (1) highlight and discuss types of
physicochemical properties relating to the bioaccumulation and toxicity of CNPs;
(2) illustrate the distribution, translocation, and speciation of CNPs under different
environmental scenarios, with an emphasis on the bioaccumulation and toxicity
outcomes; (3) discuss the phase transformation of CNPs core during interacting
with environmental components as well as the results of such transformations on
toxicity; and (4) underline the potential physiological and biochemical impacts of
CNPs and propose the related mechanisms. Finally, important knowledge gaps that
need to be addressed to better understand the potential risk, safe production, and
handling of CNPs are raised.
Surface Properties and Environmental Transformations Controlling the. . .
159