Biomedical Engineering Reference
In-Depth Information
damage in the stomach (inflammation in gastric lamina propria, submucosa, and serosa layer),
whereas 20 nm ZnO displayed a negative dose-dependent damage in the stomach (Wang et al.
2008a).
13.5.3 t
oxIcIty
of
c
opper
N
aNopartIcles
(c
opper
Np
s
)
Chen et al. investigated the oral toxicity of several types of NPs with GI tract exposure. Studies have
shown that copper NPs can cytotoxically trigger injuries on the lymph, Payer's patches, liver, spleen,
and kidney of experimental animals. In studies by Chen et al. after gavaging mice with copper NPs,
they revealed that GI tract toxicity belongs to the Hodge and Sterner scale (three classes of moderate
toxicity). Further studies revealed that the toxicity of nanosized copper particles was highly corre-
lated with the particle size and specific surface area. Compared to microcopper (17 μm), nanocop-
per (23.5 nm) can rapidly interact with artificial gastric acid juice and can be transformed into ionic
copper with an ultrahigh reactivity. They compared the toxicity of nanocopper with microcopper
in mice. A few microcopper particle-treated mice exhibited symptoms of poisoning. However, all
nanocopper-treated mice appeared to exhibit symptoms of alimentary canal disorder, such as loss
of appetite, vomiting, diarrhea, and so on. The LD50 for the nano- and microcopper particles and
cupric ions exposed to mice via oral gavage were 413, >5000, and 110 mg/kg body weight, respec-
tively. The toxicity class for both nano and ionic copper particles was class 3 (moderately toxic) and
for microcopper was class 5 (practically nontoxic) from the Hodge and Sterner scale. They also
noticed tremors or hypopnea and arching of the back in some mice that received NPs. Parameters
such as blood urea nitrogen, creatinine, total bile acid, and ALP (alkaline phosphatase) were sig-
nificantly higher than in the controls. Results indicate a gender-dependent feature of nanotoxicity.
Moreover, nanotoxicity depends on several factors, such as a huge specific surface area, ultrahigh
reactivity, and so on (Chen et al. 2006).
It has been suggested that once inside an organism's stomach, nanocopper particles could react
with protons (H
+
) from gastric juice and become quickly ionized, resulting in an overload of ionic
copper. In this case, the depletion of H
+
would then lead to a massive formation of
HCO
−
and the
induction of metabolic alkalosis (Meng et al. 2007). Nano- and microcopper exhibit different bio-
logical behaviors
in vivo
via the oral exposure route. In terms of nanocopper particles, both copper
overload and metabolic alkalosis contribute to their grave toxicity. Dissimilarly, microcopper does
not stagnate in the stomach, and the velocity of ionization is much slower than with NPs. After the
particles propelled into the small intestine by gastric emptying, the ionization reaction is prohibited
because of a basic condition and is excreted as feces. For the direct intake of copper ions, transitory
glomerulonephritis and alimentary canal disorders happen in experimental animals. These toxico-
logical responses can be partially corrected within 72 h.
The toxicity of copper particles is highly correlated to particle size and specific surface areas
because ultrahigh reactivity provokes nanocopper's
in vivo
toxicity. Nanocopper NPs may not com-
promise the mice directly; nevertheless, they lead to the accumulation of excessive alkalescent
substances and heavy metal ions (copper ions), culminating in metabolic alkalosis and copper ion
overloads. When nanocopper reacts with acid substances in the stomach, a great amount of proton
ions is consumed. Metabolic alkalosis, as well as the poisonous copper ions, cause higher mortality
than microcopper of the same dose (Meng et al. 2007).
13.5.4 t
oxIcIty
of
s
INgle
-W
alled
c
arBoN
N
aNotuBes
Smith et al. studied the toxicity of single-walled carbon nanotubes (SWCNTs) to rainbow trout.
SWCNT exposure caused a dose-dependent rise in the rate of ventilation, gill pathologies (altered
mucocytes, edema, and hyperplasia), and mucus secretion, along with SWCNT precipitation on the
gill mucus. SWCNT exposures caused a statistically significant increase in Na
+
K
+
adenosine tri-
phosphatase (ATP) activity in the gills and intestine but not in the brain (Smith et al. 2007).
