Involved in the series redox reactions, the production of ROS is another issue of
consideration. Lu et al. reported that when continued to increase the concentration of
Fe(II) from 0.6 mM, greater amount of
Á
OH was produced by CNPs in the presence
of H 2 O 2 (Lu et al. 2016). Xu et al. also proposed the generation of
Á OH by the
reaction of Fe(II) and Ce(III) species with H 2 O 2 in the bulk solution (Xu and Wang
2012). Consequently, CNPs exhibited prooxidant activity. Additionally, Ce(III) in
CNPs could transmit electrons to the iron oxide, leading to the dissolution and
dispersion of Fe(III) and Fe(II) (Wang et al. 2014). This process may further initiate
the decomposition of H 2 O 2 and eventually produce
Á OH (Xu and Wang 2012).
Consequential alterations in the physicochemical properties of CNPs during the
redox reactions between CNPs and Fe(II) can further induce the toxicity of CNPs by
mediating surface charge, dissolution of Ce(III), and generation of ROS. Besides Fe
(II), other redox reactive elements (i.e., Mn
2+ ) or contaminants (i.e., As, Cr, and U)
can also be adsorbed on and react with CNPs. These interactions need to be
considered when assessing the chemical fate and risk of CNPs in aquatic
environments.
5 Toxicity Mechanisms of CNPs Posed on the Organisms
There are several different mechanisms by which CNPs toxicants might inhibit the
growth rate of microorganism and plant in terms of cell division, since the very small
size of CNPs enables them to interact with biological systems at the subcellular scale
(membranes, proteins, or DNA molecules). Direct or physical inhibition involves
interaction of CNPs with cell itself or cytomembrane. Indirect or chemical inhibition
occurs when CNPs interact with the environment, which can be related to chemical
factors or reactions. A combination of these pathways may even be present, as
demonstrated in Fig. 5.
5.1 Physical Damage
As highlighted in the literature, the direct adsorption of CNPs onto the cell outer
membrane induces strong toxicity, and two mechanisms are probably involved.
Firstly, potential toxicity of CNPs could be caused by an interference of the adsorbed
CNPs shell with the nutrients reaching the cell surface and transport functions,
changing pH or E H in the external milieu (Rogers et al. 2010; Zeyons et al. 2009).
Secondly, upon contact with the cell membrane, the abrasive nature of CNPs was
reported to inflict non-specific physical damage. Indeed, when directly adsorbed
onto the outer cell membrane, CNPs may modify the viscosity of the membrane,
corrupt the specific ionic pumps, and thus strongly alter the transport exchanges of
the cell with the media, which interfere with the growth of both microorganisms and
plants (Rogers et al. 2010; Thill et al. 2006; van Hoecke et al. 2009; von Moos and
Slaveykova 2014).
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G. You et al.
consideration. Lu et al. reported that when continued to increase the concentration of
Fe(II) from 0.6 mM, greater amount of
Á
OH was produced by CNPs in the presence
of H 2 O 2 (Lu et al. 2016). Xu et al. also proposed the generation of
Á OH by the
reaction of Fe(II) and Ce(III) species with H 2 O 2 in the bulk solution (Xu and Wang
2012). Consequently, CNPs exhibited prooxidant activity. Additionally, Ce(III) in
CNPs could transmit electrons to the iron oxide, leading to the dissolution and
dispersion of Fe(III) and Fe(II) (Wang et al. 2014). This process may further initiate
the decomposition of H 2 O 2 and eventually produce
Á OH (Xu and Wang 2012).
Consequential alterations in the physicochemical properties of CNPs during the
redox reactions between CNPs and Fe(II) can further induce the toxicity of CNPs by
mediating surface charge, dissolution of Ce(III), and generation of ROS. Besides Fe
(II), other redox reactive elements (i.e., Mn
2+ ) or contaminants (i.e., As, Cr, and U)
can also be adsorbed on and react with CNPs. These interactions need to be
considered when assessing the chemical fate and risk of CNPs in aquatic
environments.
5 Toxicity Mechanisms of CNPs Posed on the Organisms
There are several different mechanisms by which CNPs toxicants might inhibit the
growth rate of microorganism and plant in terms of cell division, since the very small
size of CNPs enables them to interact with biological systems at the subcellular scale
(membranes, proteins, or DNA molecules). Direct or physical inhibition involves
interaction of CNPs with cell itself or cytomembrane. Indirect or chemical inhibition
occurs when CNPs interact with the environment, which can be related to chemical
factors or reactions. A combination of these pathways may even be present, as
demonstrated in Fig. 5.
5.1 Physical Damage
As highlighted in the literature, the direct adsorption of CNPs onto the cell outer
membrane induces strong toxicity, and two mechanisms are probably involved.
Firstly, potential toxicity of CNPs could be caused by an interference of the adsorbed
CNPs shell with the nutrients reaching the cell surface and transport functions,
changing pH or E H in the external milieu (Rogers et al. 2010; Zeyons et al. 2009).
Secondly, upon contact with the cell membrane, the abrasive nature of CNPs was
reported to inflict non-specific physical damage. Indeed, when directly adsorbed
onto the outer cell membrane, CNPs may modify the viscosity of the membrane,
corrupt the specific ionic pumps, and thus strongly alter the transport exchanges of
the cell with the media, which interfere with the growth of both microorganisms and
plants (Rogers et al. 2010; Thill et al. 2006; van Hoecke et al. 2009; von Moos and
Slaveykova 2014).
190
G. You et al.