Environmental Engineering Reference
In-Depth Information
silver ion fraction was higher. Flow-cytometric analyses of cell cycle and apoptosis showed that there was no significant difference
between the treatment with Ag Np suspension and Ag Np supernatant. At high silver ion fractions (≥5.5%), the Ag Np did not
add measurable toxicity to the Ag Np suspension, whereas at low silver ion fractions (≤2.6%), Ag Np suspensions were more
toxic than their supernatant [9]. Some of the manufactured nanomaterials are redox-active and are capable of passing through cell
membranes into mitochondria. Ag Nps (40 and 80 nm) can cause impairment of mitochondrial function by alterations of mito-
chondrial membrane permeability, resulting in an uncoupling effect on the oxidative phosphorylation system. Thus, the exposure
to Ag Nps causes mitochondrial toxicity, leading to cellular toxicity [11]. The physicochemical behavior, uptake, toxicity (growth
inhibition), and mechanism of toxicity of three Ag Nps with different sizes and polyvinylpyrrolidone (pVp) or citrate coatings
were characterized in the animal model
Caenorhabditis elegans
. Significant aggregation and extraorganismal dissolution of sil-
ver, organismal uptake, and transgenerational transfer of Ag Nps were observed. growth inhibition by all tested Ag Nps at con-
centrations in the low mg/l levels was seen. Although all tested Ag Nps were internalized (passed cell membranes) in
C. elegans
,
at least part of the toxicity observed was mediated by ionic silver [12]. The mechanism of action of Ag Np toxicity has also been
studied in relationship to the generation of reactive oxygen species (RoS) in A549 cells. Ag Nps caused RoS formation in the
cells, a reduction in their cell viability and mitochondrial membrane potential (mmp), an increase in the proportion of cells in
the sub-g1 (apoptosis) population, S phase arrest, and downregulation of the cell cycle-associated proliferating cell nuclear
antigen (pcNA) protein, in a concentration- and time-dependent manner. pretreatment of the A549 cells with the antioxidant
N
-acetyl-cysteine decreased the effects of Ag Nps on the reduced cell viability, caused changes in the mmp and proportion of
cells in the sub-g1population, but had no effect on the Ag Np-mediated S phase arrest or downregulation of pcNA. Thus, it
could be concluded that the
in vitro
toxic effects of Ag Nps on A549 cells were mediated by both RoS-dependent (cytotoxicity)
and RoS-independent (cell cycle arrest) pathways [10]. The effect of particle size on Ag Nps' cytotoxicity, inflammation, geno-
toxicity, and developmental toxicity revealed that Ag Nps of 20 nm were more toxic than the larger nanoparticles. However,
20 nm sized Ag Nps were more cytotoxic in comparison to silver ions in l929 fibroblasts than in but not in RAW 264.7 macro-
phages. This implies that the potency of silver to induce cell damage depends on both the cell type and and its size [13].
Ag Nps can also induce stress responses along with cytotoxicity in mammalian cells. Ag Nps are efficiently internalized via
scavenger receptor-mediated phagocytosis in murine macrophages, get localized in the cytoplasm, cause mitochondrial
damage, and induce apoptosis and cell death. in the presence of Ag ion-reactive thiol-containing compounds, these effects are
more, which implies that Ag ions play a major role in Ag Np toxicity. Ag Nps are internalized by scavenger receptors, trafficked
to the cytoplasm, and induce toxicity by releasing Ag ions [14]. in another study, Ag Nps synthesized by reduction with tannic
acid (TSNps) and sodium borohydride were assessed for toxicity in a cellular environment using skin epithelial A431, lung
epithelial A549, and murine macrophage RAW264.7 cells over a range of doses (5-100 µg/ml). TSNps exhibited a higher neg-
ative zeta-potential and also higher toxicity and dose-dependent increase in RoS generation and cellular disruption. TSNps
induced a dose-dependent increase in the expression of stress markers pp38, TNF-α, and HSp-70. The toxicity of nanoparticles
was found to vary according to their surface potential. This proves that the cytotoxicity of Ag Nps changes with the surface
potential of nanoparticles and cell type. Thus, physicochemical properties of Ag Nps direct their toxicity [15].
31.3.2
gold nanoparticles
gold nanoparticles (Au Nps) offer great promise in biomedical applications. Au Nps have shown promising biological and
military applications due to their unique electronic and optical properties. Au Nps are usually considered to be bioinert, but
questions have been raised regarding their safety. However, little is known about their cytotoxicity when they come into contact
with a biological system. Hence, it is essential to study the cytotoxicity of Au Nps. Au Nps are able to cross the blood-brain
barrier and accumulate in the neural tissue. However, no evidence of toxicity was observed on evaluating the bioaccumulation
and toxic effects of different doses (40, 200, and 400 µg/kg/day) of 12.5 nm Au Nps upon intraperitoneal administration in mice
every day for 8 days. The gold levels in blood did not increase with the dose administered, whereas in all the organs examined
there was a proportional increase in gold, indicating efficient tissue uptake. Thus, tissue accumulation patterns of Au Nps
depend on the doses administered and the accumulation of the particles does not produce subacute physiological damage [16].
in another study, Balb/3T3 mouse fibroblasts were exposed to Au Nps (5 and 15 nm) citrate stabilized for 72 h. only Au Nps
5 nm in size at concentrations ≥50 μm exhibited cytotoxic effects. Disruption of the actin cytoskeleton was evident and reduction
of the expression and degradation of the clathrin heavy chain were observed in cells exposed for 72 h to Au Nps [17]. it has been
shown that small Au Nps can be endocytosed by cells and form aggregates inside the cell, resulting in cytotoxicity [31]. The
interaction of Au Nps with glutathione (gSH) and their role in the sequence of apoptotic signaling events that occur after mod-
ulation of the cellular redox state were studied in Hl7702 cells (human liver cell line). After incubation with 8 nm AuNps at
50 nm, there was an early decline in cytosolic gSH, which initiated mitochondrial transmembrane potential depolarization and
apoptosis. Au Nps (8 nm) possess strong Au-S bonding interactions with gSH resulting in intracellular gSH depletion.
