133
nanotubes exposed ones had less viability indices. A recent review suggested that
the placenta does not provide a tight barrier against the transfer of nanoparticles to
fetuses, specifically against the distribution of carbonaceous nanoparticles to and in
the fetus. (Ema et al. 2016).
Silica Nanoparticles
Comprehensive production and use of silica nanoparticles have increased the risk of
human exposure. For this reason, safety of silica nanoparticles is a major issue.
Silica nanoparticles are widely used in construction, catalysis, paints (pigments)
and pharmaceutical applications, agriculture, food, and consumer products. The
health effects of silica, especially crystalline silica (0.5–10μm) on human have
widely been studied. Occupational exposure to crystalline silica induces a fibrotic
lung disease, also called silicosis, in workers and also causes emphysema and pulmonary tuberculosis. On the contrary, natural amorphous silica is generally less
harmful than crystalline silica (Murugadoss et al. 2017).
Animal inhalation studies were carried out with silica nanoparticles to assess the
effects of silica nanoparticles on blood biochemical parameters and changes on
pathology and histology. Silica nanoparticles caused the transient changes on
breathing parameters, increased lung weight, total bronchoalveolar lavage cells and
proteins, induced acute inflammation and tissue damage. Liver is key tissue for silica nanoparticles toxicity. The lactate dehydrogenase (LDH) level in exposed mice
was found significantly higher than controls, and the alanine transaminase (ALT)
levels were also increased. All these elevation as indicate cell membrane injury and
tissue damage. For aspartate aminotransferase (AST), it was observed little elevation and no any increase was observed with serum albumin, blood urea nitrogen
(BUN), and creatinine levels. Lymphocytic infiltration, granuloma formation, and
hydropic degeneration in the hepatocytes were observed in the livers. It indicated
that the silica nanoparticles may be hepatotoxic. Pulmonary hyperemia and pulmonary interstitial thickening were observed (Yu et al. 2013).
Silica nanoparticles caused hepatotoxicity however possible mechanisms of hepatotoxicity still remain unclear. Ahmad et al. investigated the toxic effects of silica
nanoparticles on liver. They designed a series of experiments on human liver cell
line HepG2 to clarify the hepatotoxicity mechanism of silica nanoparticles. They
explored that silica nanoparticles (14 nm) causes apoptosis via reactive oxygen species. Silica nanoparticles also leads to oxidative stress through reactive oxygen species production and lipid peroxidation and thereby depletion of glutathione. Whereas
mRNA and protein expressions of cell cycle checkpoint gene p53 and apoptotic
genes (bax and caspase-3) were upregulated and antiapoptotic gene was down regulated in exposed mice. All these results contributed to hepatotoxicity mechanisms of
silica nanoparticles (Ahmad et al. 2012).
Nanoparticles of Polymeric Materials
Polymer-based nanoparticle is a collective term which is given to any kind of
polymer- based nanoparticle, but specifically is applied for nanospheres and nanocapsules. Polymer-based nanoparticle is used and have roles in photonics, electronics, sensors, medicine, pollution control, and environmental technology (Mallakpour
5 Nanomaterials Causing Cellular Toxicity and Genotoxicity
nanotubes exposed ones had less viability indices. A recent review suggested that
the placenta does not provide a tight barrier against the transfer of nanoparticles to
fetuses, specifically against the distribution of carbonaceous nanoparticles to and in
the fetus. (Ema et al. 2016).
Silica Nanoparticles
Comprehensive production and use of silica nanoparticles have increased the risk of
human exposure. For this reason, safety of silica nanoparticles is a major issue.
Silica nanoparticles are widely used in construction, catalysis, paints (pigments)
and pharmaceutical applications, agriculture, food, and consumer products. The
health effects of silica, especially crystalline silica (0.5–10μm) on human have
widely been studied. Occupational exposure to crystalline silica induces a fibrotic
lung disease, also called silicosis, in workers and also causes emphysema and pulmonary tuberculosis. On the contrary, natural amorphous silica is generally less
harmful than crystalline silica (Murugadoss et al. 2017).
Animal inhalation studies were carried out with silica nanoparticles to assess the
effects of silica nanoparticles on blood biochemical parameters and changes on
pathology and histology. Silica nanoparticles caused the transient changes on
breathing parameters, increased lung weight, total bronchoalveolar lavage cells and
proteins, induced acute inflammation and tissue damage. Liver is key tissue for silica nanoparticles toxicity. The lactate dehydrogenase (LDH) level in exposed mice
was found significantly higher than controls, and the alanine transaminase (ALT)
levels were also increased. All these elevation as indicate cell membrane injury and
tissue damage. For aspartate aminotransferase (AST), it was observed little elevation and no any increase was observed with serum albumin, blood urea nitrogen
(BUN), and creatinine levels. Lymphocytic infiltration, granuloma formation, and
hydropic degeneration in the hepatocytes were observed in the livers. It indicated
that the silica nanoparticles may be hepatotoxic. Pulmonary hyperemia and pulmonary interstitial thickening were observed (Yu et al. 2013).
Silica nanoparticles caused hepatotoxicity however possible mechanisms of hepatotoxicity still remain unclear. Ahmad et al. investigated the toxic effects of silica
nanoparticles on liver. They designed a series of experiments on human liver cell
line HepG2 to clarify the hepatotoxicity mechanism of silica nanoparticles. They
explored that silica nanoparticles (14 nm) causes apoptosis via reactive oxygen species. Silica nanoparticles also leads to oxidative stress through reactive oxygen species production and lipid peroxidation and thereby depletion of glutathione. Whereas
mRNA and protein expressions of cell cycle checkpoint gene p53 and apoptotic
genes (bax and caspase-3) were upregulated and antiapoptotic gene was down regulated in exposed mice. All these results contributed to hepatotoxicity mechanisms of
silica nanoparticles (Ahmad et al. 2012).
Nanoparticles of Polymeric Materials
Polymer-based nanoparticle is a collective term which is given to any kind of
polymer- based nanoparticle, but specifically is applied for nanospheres and nanocapsules. Polymer-based nanoparticle is used and have roles in photonics, electronics, sensors, medicine, pollution control, and environmental technology (Mallakpour
5 Nanomaterials Causing Cellular Toxicity and Genotoxicity