Environmental Engineering Reference
In-Depth Information
96 h of treatment. Hence, Tio
2
Nps have a cytotoxic effect on glial cells, suggesting that exposure to Tio
2
Nps could cause
brain injury and be hazardous to health [22]. Exposure to Tio
2
Nps has been demonstrated to result in pulmonary inflam-
mation in animals. The oxidative stress and molecular mechanism associated with pulmonary inflammation in chronic lung
toxicity caused by the intratracheal instillation of Tio
2
Nps for 90 consecutive days in mice were evaluated. Tio
2
Nps sig-
nificantly accumulated in the lung, leading to an obvious increase in lung indices, inflammation, and bleeding in the lung.
Exposure to Tio
2
Nps significantly increased the accumulation of RoS and the level of lipid peroxidation, and decreased
antioxidant capacity in the lung. Furthermore, Tio
2
Nps exposure activated nuclear factor-κB (NF-κB), increased the levels
of tumor necrosis factor-α, cyclooxygenase-2, heme oxygenase-1, interleukin-2, interleukin-4, interleukin-6, interleukin-8,
interleukin-10, interleukin-18, interleukin-1β, and cyp1A1 expression. However, Tio
2
Np exposure decreased
NF-κB-inhibiting factor and heat shock protein 70 expression. Thus, the generation of pulmonary inflammation caused by
Tio
2
Nps in mice is closely related to oxidative stress and the expression of inflammatory cytokines [23]. The long-term
risk of Tio
2
Np exposure was studied by using zebrafish (
Danio rerio
) as
in vivo
model to assess the chronic toxicity of
Tio
2
Nps. The adverse effect to zebrafish was seen as concentration-dependent and time-dependent inhibition of growth
and decrease in the liver weight ratio of zebrafish. Tio
2
Nps could translocate among organs and pass through the blood-
brain and the blood-heart barrier after long-term exposure and accumulate and get distributed in gill, liver, heart, and brain
[24]. Tio
2
Nps are also known to damage the kidney of mice on exposure. The molecular mechanism of Tio
2
Nps-induced
nephric injury has been investigated. Tio
2
Nps accumulate in the kidney, resulting in nephric inflammation, cell necrosis,
and dysfunction. NF-κB gets activated by Tio
2
Np exposure, promoting the expression levels of tumor necrosis factor-α,
macrophage migration inhibitory factor, interleukin-2, interleukin-4, interleukin-6, interleukin-8, interleukin-10, inter-
leukin-18, interleukin-1β, cross-reaction protein, transforming growth factor-β, interferon-γ, and cyp1A1. Thus, Tio
2
Np-induced nephric injury of mice is associated with alteration of inflammatory cytokine expression and reduction of
detoxification of Tio
2
Nps [25].
31.3.5
silicon dioxide nanoparticles
Silica nanoparticles (nano-Sio
2
) are one of the most popular nanomaterials used in industrial manufacturing and medicine.
While inhalation of nanoparticles causes pulmonary damage, nano-Sio
2
can be transported into the blood and get deposited in
target organs where they exert potential toxic effects. The kidney is one such secondary target organ. However, toxicological
information of their effect on renal cells and the mechanisms involved remain sparse. on investigating the cytotoxicity of
nano-Sio
2
of different sizes on two renal proximal tubular cell lines (human Hk-2 and porcine llc-pk
1
), it was shown that
internalization process occurs by macropinocytosis and clathrin-mediated endocytosis for 100 nm nano-Sio
2
. These nanopar-
ticles were localized in vesicles. Toxicity was size- and time-dependent (24, 48, 72 h) and increased as nanoparticles became
smaller. Second, analysis of oxidative stress based on the assessment of RoS production (dihydroethidium) or lipid peroxi-
dation (malondialdehyde) clearly demonstrated the involvement of oxidative stress in the toxicity of 20 nm nano-Sio
2
.
The induction of antioxidant enzymes (catalase, gSTpi, thioredoxin reductase) could explain their lesser toxicity with 100 nm
nano-Sio
2
[26].
31.3.6
copper oxide nanoparticles
copper oxide nanoparticles (cuo Nps) are increasingly used in various applications. oxidative stress is considered to be the
main cause of the cytotoxicity of cuo Nps in mammalian cells. However, little is known about the mechanism of genotoxicity
of cuo Nps following exposure to human cells. cuo Nps were known to induce genotoxic response through p53 pathway in
human pulmonary epithelial cells (A549). cuo Nps reduced cell viability and the degree of reduction was dose-dependent.
cuo Nps were also found to induce oxidative stress in a dose-dependent manner indicated by depletion of glutathione and
induction of lipid peroxidation, catalase, and superoxide dismutase. The expression of Hsp70, the first-tier biomarker of cellular
damage, was induced by cuo Nps. Further, cuo Nps upregulated the cell cycle checkpoint protein p53 and the expression of
DNA damage repair proteins Rad51 and mSH2. These results demonstrate that cuo Nps possess a genotoxic potential in A549
cells that may be mediated through oxidative stress [27]. To assess the toxicity of cuo Nps (23.5 nm)
in vivo
, lD
50
, morpho-
logical changes, pathological examinations, and blood biochemical indexes of experimental mice were studied comparatively
with microcopper particles (17 µm) and cupric ions (cucl
2
·2H
2
o). The lD
50
for the cuo Nps, microcopper particles, and cupric
ions exposed to mice via oral gavage were 413, >5000, and 110 mg/kg body weight, respectively. The toxicity classes of nano
and ionic copper particles are both class 3 (moderately toxic), and microcopper is class 5 (practically nontoxic) on the Hodge
and Sterner Scale. The kidney, liver, and spleen were found to be target organs of cuo Nps. Nanoparticles induced toxicolog-
ical effects and heavy injuries on the kidney, liver, and spleen of experimental mice, but microcopper particles did not, on a mass
