Environmental Engineering Reference
In-Depth Information
A decrease in gSH alone can act as a potent early activator of apoptotic signaling. increased H
2
o
2
production following
mitochondrial gSH depletion represents a crucial event, which commits Hl7702 cells to apoptosis through the mitochondrial
pathway [18]. To understand the long-term consequences of developmental nanoparticle exposure, zebrafish embryos were
acutely exposed to three Au Nps that possess functional groups with differing surface charges. Embryos were exposed to 50 µg/
ml of 1.5 nm Au Nps possessing negatively charged 2-mercaptoethanesulfonic acid (mES), neutral 2-(2-(2-mercaptoethoxy)
ethoxy)ethanol (mEEE) ligands, and positively charged 10 µg/ml of the Au Nps containing trimethylammoniumethanethiol
(TmAT). Both mES-Au Np- and TmAT-Au Np-exposed embryos exhibited hypolocomotor activity, while those exposed to
mEEE-Au Nps did not. A subset of embryos that were exposed to 1.5 nm mES-Au Nps and TmAT-Au Nps during development
from 6 to 120 h post fertilization were raised to adulthood. Behavioral abnormalities and the number of survivors into adulthood
were evaluated at 122 days post fertilization. it was found that both treatments induced abnormal startle behavior following a
tap stimulus. However, the mES-Au Nps-exposed group also exhibited abnormal adult behavior in light and had a lower
survivorship into adulthood. Thus, acute, developmental exposure to 1.5 nm mES-Au Nps and TmAT-Au Nps, two nanopar-
ticles differing only in the functional group, affects larval behavior, with effects of behavior persisting into adulthood [19].
Thus, it is clear that long-term retention of Au Nps in the body increases the potential for toxicity. However, it was shown in
a recent study that nanoclustering of gold and iron as a nanoparticle could be easily biodegraded in lysosomes of macrophages.
on administering nanorose (nanoclustered gold and iron nanoparticle) to c57Bl/6 mice, the gold concentration was signifi-
cantly reduced in 11 murine tissues in as few as 31 days (
P
< 0.01). moreover, the hematology studies showed no toxicity of
nanorose injected into mice for up to 14 days after administration. This implies that degradation of nanoparticles into smaller
subunits can enhance and facilitate their rapid excretion. Therefore, such strategies to decrease the particle size for excretion
can reduce the potential toxicity of Au Nps [32].
31.3.3
Zinc oxide nanoparticles
Zinc oxide nanoparticles (Zno Nps) are finding applications in a wide range of products including cosmetics, food packaging,
and antimicrobial coatings. Therefore, there are high chances of human exposure to these nanoparticles through dermal, inhala-
tion, and oral routes. Toxicity studies on the effect of Zno Nps on ecological receptors across different taxa such as bacteria,
algae and plants, as well as aquatic and terrestrial invertebrates and vertebrates have shown that relatively high to acute toxicity
of Zno Nps (in the low mg/l levels) to environmental species is highly dependent on test species, physicochemical properties of
the material, and test methods. particle dissolution to ionic zinc and particle-induced generation of RoS represented the primary
modes of action for Zno Np toxicity across all species tested, and photoinduced toxicity associated with its photocatalytic prop-
erty was the other important mechanism of toxicity under environmentally relevant uV radiation [33]. Studies on oral toxicity of
Zno Nps in mice revealed that a significant accumulation of nanoparticles in the liver leads to cellular injury after subacute oral
exposure of Zno Nps (300 mg/kg) for 14 consecutive days. This was evident by the elevated alanine aminotransferase (AlT) and
alkaline phosphatase (Alp) serum levels and pathological lesions in the liver. Zno Nps were also found to induce oxidative stress
indicated by an increase in lipid peroxidation. Fpg-specific DNA lesions were observed in the liver, indicating that oxidative
stress was the cause of DNA damage. Subacute oral exposure to Zno Nps in mice leads to an accumulation of nanoparticles in
the liver, causing oxidative stress-mediated DNA damage and apoptosis. These results also suggest the need for a complete risk
assessment of any new engineered nanoparticle before its arrival into the consumer market [20].
Similarly, in a study focusing on the cyto- and genotoxicity of Zno Nps and Zno powder in primary human nasal mucosa
cells cultured in the air-liquid interface, cytotoxic effects and DNA damage were shown at a Zno Np concentration of 50
(
P
< 0.01) and 10 µg/ml (
P
< 0.05), respectively. This indicates cyto- and genotoxic properties as well as a proinflammatory
potential of Zno Nps in nasal mucosa cells. Therefore, precautionary measures should be taken before wide-scale industrial
and dermatological application of these nanoparticles. However, further investigations on long-term exposure to Zno Nps are
required to understand their impact on the environment and human health [21].
31.3.4
titanium dioxide nanoparticles
Titanium dioxide nanoparticles (Tio
2
Nps) are an important material used as an additive in pharmaceutical and cosmetic
products. Due to their high surface-to-mass index, Tio
2
Nps show unique physical and chemical characteristics compared
to the bulk substance [34]. Tio
2
Nps are widely used in the chemical, electrical, and electronic industries. They can enter
directly into the brain through the olfactory bulb and get deposited in the hippocampus region. The effect of Tio
2
Nps on
rat and human glial cells, c6 and u373, has been studied to understand their mechanism of action in the nervous system.
Tio
2
Nps inhibited proliferation and induced morphological changes that were related with a decrease in immunolocation
of F-actin fibers. Tio
2
Nps were internalized and the formation of vesicles was observed. Tio
2
Nps induced apoptosis after