Biomedical Engineering Reference
In-Depth Information
the copper nanoparticles induced kidney toxicity and cell death via the activation of oxidative and
nitrosative-stress responsive cell signaling. They observed that the exposure to copper nanoparticles
increased the intracellular ROS and NO production in a dose-dependent manner. Both oxidative
and nitrosative stress altered enzymatic and nonenzymatic antioxidant defenses. They assayed the
activities of the antioxidant enzymes SOD (superoxide dismutase), CAT (catalase), GST (gluta-
thione
S
-transferase), GR (glutathione reductase), GPx (glutathione peroxidase), and the levels of
the nonenzymatic antioxidant molecules GSH (glutathione) and its metabolite GSSG (glutathione
disulfide) and observed that the overload of intracellular copper nanoparticles decreased the activi-
ties of antioxidant enzymes and levels of GSH, along with increased GSSG, lipid peroxidation, and
protein carbonylation. Since vitamin E treatments can prevent all these alterations related to oxida-
tive stress induced by copper nanoparticles, it was concluded that ROS play a major role in copper
nanoparticle-induced renal toxicity (Sil et al. 2011).
14.3.4.3 Toxicity of Gold Nanoparticles
Studies have shown that gold is heavily taken up by the kidneys, causing nephrotoxicity and also ini-
tiating eryptosis (erythrocyte suicidal death) (Sereemaspun et al. 2008; Sopjani et al. 2008). Studies
have suggested that the size, shape, and surface charge are key factors related to the potential toxic-
ity of medicinal gold complexes.
Gold nanoparticles produced occasional glomerular congestion in rats exposed to 10 or 20 nm
particles for 7 days, but not in the glomeruli of rats exposed to 50 nm particles. The occasional
dilatation of glomerular tuft blood capillaries was observed (Mohamed and Bashir 2011). Terentyuk
et al. reported the proliferation of Bowman's capsule epithelial cells by gold nanoparticles, where
15 nm particles showed more effect than larger ones (Terentyuk et al. 2009). Renal tubules' epi-
thelial lining exhibited cloudy swellings with pale cytoplasms and poorly delineated and displaced
nuclei in all gold nanoparticle-treated rats. This alteration was more prominent in the proximal con-
voluted tubules than the distal ones, with more swelling induced by the 100 μL dose than the 50 μL
dose, and with 10 and 20 nm-sized particles than larger ones. Cytoplasmic swelling might be exhib-
ited as a result of disturbances in membrane functions that lead to the massive influx of water and
Na
+
due to the effects of gold nanoparticles. This alteration might be accompanied by the leakage of
liposome hydrolytic enzymes that lead to cytoplasmic degeneration and macromolecular crowding
(Del 2005; Mohamed and Bashir 2011). Anisokaryosis (variable nuclei sizes) were observed in some
renal cells. This change became noticeable 7 days after the administration of 50 nm gold nanopar-
ticles. Several studies indicate that nuclear polymorphisms are seen in dysplasia and carcinomatous
lesions (Zusman et al. 1991; Mohamed and Bashir 2011). Sections of gold nanoparticle-treated kid-
neys developed pyknosis in some epithelial cells of the proximal tubules with a lesser extent in the
distal ones. This alteration was seen in all 10 and 20 nm gold nanoparticle-treated rats. Pyknotic
nuclei exhibited the clumping and condensation of chromatin material in the periphery of the nuclei,
together with the irregularity of nuclear membranes (Kumar et al. 2007; Mohamed and Bashir
2011). Histological alterations through the exposure of gold nanoparticles could be an indication
of injured renal tissue due to toxicity that becomes unable to deal with as well as the accumulated
residues resulting from metabolic and structural disturbances caused by gold particles. One might
conclude that these alterations are size dependent, as smaller ones induced more damage to renal
tissue with relation to gold nanoparticle exposure time. This might be due to the earlier accumula-
tion of larger nanoparticles in the tissue while the smaller ones stay in the blood stream much longer
due to recirculation (Mohamed and Bashir 2011).
14.3.4.4 Toxicity of Carbon Nanotubes
Reddy et al. found that the exposure to carbon nanoparticles at dosage levels of 3-300 μg/mL caused
a dose-dependent cytotoxicity as revealed by mitochondrial function (MTT assay). It was found
that the higher cytotoxicity of both nanoparticles was comparable with known cytotoxic agent and
quartz (positive control) against all cell type tested. The IC
50
values of both carbon nanoparticles
