form colloidal complex after interaction with organic materials like proteins, humic and fulvic acids, and inorganic
species notably hydrous manganese, iron oxides. Further, to
interpret the future usage of nano-fertilizers, a huge amount
of N and P in nanoform is going to be released in the water
bodies, which may affect the ecosystem and human health.
Consequences of these interactions are completely unknown
(Ma et al. 2014; Johnson et al. 2014; Yang et al. 2015). It is
estimated that occurrence of NPs in aquatic system is quite
low in comparison with the natural NPs (Delay and Frimmel
2012). Therefore, the movement and translocation of NPs
within waters are a budding issue. Nano-pollution in aquatic
body is a major cause of concern, and there are few reports
available which have specifically dealt to remediate the
nano-contamination in the water bodies. In one study published recently, it is reported that iron oxide nanoparticles
can be accumulated inside the green algae Coelastrella
terrestris. In this way, remediation of water containing
excess NPs is possible. The accumulation factor reported in
this study was found to be about 2.9, which means, about 2.9
times iron oxide NP is accumulated inside the algal cell than
ambient environment (Saxena et al. 2020). It has been
reported that NPs affect the life of aquatic ecosystem by
inhibiting growth and nitrogen fixing capacity, increasing
the level of ROS and MDA, decreasing the pigment content
in photosynthesis organisms, negatively influencing antioxidant enzymes. Further, physical damage to subcellular
organs like membrane damage, cell wall damage and
intra-thylakoidal damage are also reported (Saxena and
Harish 2018).
3 Toxicity Mechanisms of Nanoparticles
3.1 Proposed Mode of Antibacterial Action
of Metal Nanoparticles
It is widely known that metal NPs such as AgNPs and
CuNPs have significant antibacterial activity (Table 1), but
the mechanism of their action is yet not known. There is
some literature available on metal NPs mode of action, but
until now, the mode of action is very unclear. Das et al.
(2010) reported that CuNPs are capable of entering the cell
because of their smaller size and subsequently takes place
their protein or enzyme inactivation, producing hydrogen
peroxide that results in the death of bacterial cells. In another
report, it has been stated that the protein inactivation occurs
because of the CuNPs and –SH group of proteins interaction
with each other (Schrand et al. 2010). Likewise, metal NPs
can disturb the DNA helical structure and degrade it. The
cell membrane integrity is decided by the electrochemical
potential, since according to Deryabin et al. (2013), CuNPs
are responsible to reduce the cell membranes
electrochemical potential, that eventually affected the cell
membrane integrity. It was also understood that metal NPs
liberate their respective ions, and these heavy metal ions are
found to have unfavourably affected the cells of bacteria
(Cioffi et al. 2005). Metal NPs and metal ions accumulation
on surface of cell cause the formation of pits in the membrane, which mainly leading to the outflow of components
from bacterial cells ultimately causing the cells death. The
next significant reason for the bacterial cell death has been
proposed is the oxidative stress development due to the
action of NPs (Deryabin et al. 2013). Considering all these
possibilities, Shende et al. (2015) have proposed a hypothetical mechanism of action of CuNPs in bacteria; in a
similar way, metal NPs could impact the bacterial cells
during the bactericidal action (Fig. 1).
3.2 Proposed Mechanism of Antifungal Action
of Metal Nanoparticles
The mechanistic action of metal NPs as a fungicidal agent is
still unclear; however, there are many ways by which metal
NPs could serve as an antifungal agent depending on their
mode of action. The probable antifungal action of metal NPs
could be correlated with the commercial fungicides available
in the market (Fig. 2).
Although the commercially available antifungal agents
are target specific and are mainly limited to the plasma
membrane and cell wall, which are the targets (Ngo et al.
2016; Scorzoni et al. 2017), the metal NPs which were
capped with proteins in case of biogenic synthesize could get
attached to the fungal cell wall and initiate a sustainable
release of the metal ions inside the cell, which can act on the
fungi by different ways.
A lipid responsible for membrane fluidity is ergosterol
and essential for cell viability (Tatsumi et al. 2013; Song
et al. 2016). A few antifungal agents generally target
ergosterol, either by restraining its biosynthesis or binding to
it, resulting in the formation of the pores in the membrane,
this may be similar to the metal NPs or metal ions. The
composition of fungal cell wall primarily constituted chitin,
mannans, glycoproteins and glucans, essential for adhesion
and pathogenesis of fungi and also provides a protective
barrier, limiting the admittance of molecules to the plasma
membrane (van der Weerden et al. 2013).
The two most important modes of action of antifungal
agents targeting the cell wall are associated with the inhibition of chitin and b-glucan synthesis. Thus, metal NPs may
perhaps target chitin synthase, which is responsible for the
chitin chain elongation. Another mechanism is inhibition of
nucleic acids, protein and microtubule synthesis. There are
some antifungals, which may cause more than one effect on
the fungal cells under adverse conditions, like in the
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