2.1 Size
The various sizes of CNPs can be achieved by specific synthesis methods. For
example, wet chemical and microemulsion methods provide satisfactory control
over CNPs size, with the former yielding CNPs of small particle size (Das et al.
2012; Tarnuzzer et al. 2005). The latter one may produce dense and crystalline CNPs
with large particle size (>25 nm) (Zhang et al. 2011). However, the change of
particle size would affect the interactions at CNPs-biological interface. As exhibited
in Table 1, there exist numerous toxicity studies suggesting the significance of size in
toxicity and verifying that nanoscale is the prime cause in toxicity induction, since
smaller CNPs were found to be more toxic against algae (Rogers et al. 2010),
Caenorhabditis elegans (Roh et al. 2010), Brassica rapa (Ma et al. 2016), Cucurbita
pepo L. (Hawthorne et al. 2014), E. coli, and B. subtilis (Pelletier et al. 2010) than the
larger ones. Due to comparable size with the biomacromolecules (Hassan et al. 2016;
Limbach et al. 2005; van Hoecke et al. 2009), the intake of smaller CNPs occurs
easily, thus inducing the oxidative stress as well as physiological damage inside the
cellular environment (Ma et al. 2016; Park et al. 2008b; Pešić et al. 2015). On the
contrary, it was demonstrated that the size of CNPs did not show any measurable
correlation with algae and kidney bean plants’ (Phaseolus vulgaris) growth inhibition (Majumdar et al. 2016a, b; Pulidoreyes et al. 2015). Surprisingly, larger CNPs
were reported to show higher toxicity to eukaryotic cells than smaller ones (Schubert
et al. 2006), as reported by Dahle (2013). Similarly, Park et al. observed that 30 nm
CNPs displayed toxic effects toward BEAS-2B cells (Park et al. 2008b), while at the
same concentration, Fang et al. illustrated that 13 nm CNPs induced no cytotoxicity
in the same cell line (Fang et al. 2010). This phenomenon could be attributed to the
greater agglomeration tendency of the smaller-sized CNPs than the larger ones,
which sequestrated their reactions reactivity and thus toxicity in the individual
exposure medium (Dahle 2013; Hamidat et al. 2017; Kumar et al. 2014).
In another analysis, authors explored the effects of size on the conversion
between antioxidant and prooxidant activity of CNPs. The study found that at the
same concentration of 10 μM, 15–20 nm CNPs had excellent antioxidant ability and
thus an obvious protection effect, whereas CNPs (5–10 nm) behaved in the opposite
manner (Lu et al. 2016). In contrast, Auffan et al. detected that 7 nm CNPs induced
DNA damage in human dermal fibroblasts (Auffan et al. 2017a) and the formation of
ROS in human dermal fibroblasts was confirmed by Culcasi et al. under the same
conditions (Culcasi et al. 2012). Nevertheless, Karakoti et al. demonstrated the
antioxidant activity of 4 nm CNPs in human dermal fibroblasts (Karakoti et al.
2009). These conflicting findings illustrate that CNPs with only different sizes
perform differently, even at the same dosage in the same system.
Generally, to estimate the size effects of CNPs and to draw general conclusions,
different susceptibility, varying feeding habits, and metabolism among tested species are vital factors that need to be taken into account. Importantly, when concluding the size effects of CNPs, factors including CNPs internalization, agglomeration,
and surface property need to be comprehensively considered. Also, subcellular
location and surface reactivity of CNPs controlled by their particle size can be
detrimental to cells, which are still less understood.
Surface Properties and Environmental Transformations Controlling the. . .
169
The various sizes of CNPs can be achieved by specific synthesis methods. For
example, wet chemical and microemulsion methods provide satisfactory control
over CNPs size, with the former yielding CNPs of small particle size (Das et al.
2012; Tarnuzzer et al. 2005). The latter one may produce dense and crystalline CNPs
with large particle size (>25 nm) (Zhang et al. 2011). However, the change of
particle size would affect the interactions at CNPs-biological interface. As exhibited
in Table 1, there exist numerous toxicity studies suggesting the significance of size in
toxicity and verifying that nanoscale is the prime cause in toxicity induction, since
smaller CNPs were found to be more toxic against algae (Rogers et al. 2010),
Caenorhabditis elegans (Roh et al. 2010), Brassica rapa (Ma et al. 2016), Cucurbita
pepo L. (Hawthorne et al. 2014), E. coli, and B. subtilis (Pelletier et al. 2010) than the
larger ones. Due to comparable size with the biomacromolecules (Hassan et al. 2016;
Limbach et al. 2005; van Hoecke et al. 2009), the intake of smaller CNPs occurs
easily, thus inducing the oxidative stress as well as physiological damage inside the
cellular environment (Ma et al. 2016; Park et al. 2008b; Pešić et al. 2015). On the
contrary, it was demonstrated that the size of CNPs did not show any measurable
correlation with algae and kidney bean plants’ (Phaseolus vulgaris) growth inhibition (Majumdar et al. 2016a, b; Pulidoreyes et al. 2015). Surprisingly, larger CNPs
were reported to show higher toxicity to eukaryotic cells than smaller ones (Schubert
et al. 2006), as reported by Dahle (2013). Similarly, Park et al. observed that 30 nm
CNPs displayed toxic effects toward BEAS-2B cells (Park et al. 2008b), while at the
same concentration, Fang et al. illustrated that 13 nm CNPs induced no cytotoxicity
in the same cell line (Fang et al. 2010). This phenomenon could be attributed to the
greater agglomeration tendency of the smaller-sized CNPs than the larger ones,
which sequestrated their reactions reactivity and thus toxicity in the individual
exposure medium (Dahle 2013; Hamidat et al. 2017; Kumar et al. 2014).
In another analysis, authors explored the effects of size on the conversion
between antioxidant and prooxidant activity of CNPs. The study found that at the
same concentration of 10 μM, 15–20 nm CNPs had excellent antioxidant ability and
thus an obvious protection effect, whereas CNPs (5–10 nm) behaved in the opposite
manner (Lu et al. 2016). In contrast, Auffan et al. detected that 7 nm CNPs induced
DNA damage in human dermal fibroblasts (Auffan et al. 2017a) and the formation of
ROS in human dermal fibroblasts was confirmed by Culcasi et al. under the same
conditions (Culcasi et al. 2012). Nevertheless, Karakoti et al. demonstrated the
antioxidant activity of 4 nm CNPs in human dermal fibroblasts (Karakoti et al.
2009). These conflicting findings illustrate that CNPs with only different sizes
perform differently, even at the same dosage in the same system.
Generally, to estimate the size effects of CNPs and to draw general conclusions,
different susceptibility, varying feeding habits, and metabolism among tested species are vital factors that need to be taken into account. Importantly, when concluding the size effects of CNPs, factors including CNPs internalization, agglomeration,
and surface property need to be comprehensively considered. Also, subcellular
location and surface reactivity of CNPs controlled by their particle size can be
detrimental to cells, which are still less understood.
Surface Properties and Environmental Transformations Controlling the. . .
169