Biomedical Engineering Reference
In-Depth Information
useful for assessing the toxicity of NPs (Henry et al. 2007; Park et al. 2010, 2011 ). Therefore, the
primary objective of the study was to make an initial assessment on the effects of dietary copper
nanoparticles or silver nanoparticles (Cu-NPs or Ag-NPs) on gut microbial communities in adult
zebrafish. In addition, to evaluate gut microbiota, the presence of lesions in the intestinal epithelial
mucosa after exposure to NPs was assessed by electron microscopy. While the uses of Cu-NPs are
emerging, they do not currently present substantial exposure risks to organisms; on the other hand,
Cu is an important environmental toxicant and the selection of Cu-NPs for this study was based on
the interest to compare results with Ag-NPs, evaluate differences between nano- and bulk forms
of Cu, and to enable comparisons with the previous studies of Cu-NPs (Griffitt et al. 2007; Shaw
et al. 2012).
NPs can be ingested by organisms, and those with antimicrobial properties may disrupt benefi-
cial endogenous microbial communities and affect the health of the organism. Zebrafish was fed
with diets containing Cu-NPs, Ag-NPs (500 mg/kgfood), or an appropriate control for 14 days.
By transmission electron microscopy (TEM), the intestinal epithelium integrity was examined
and the structure of the microbial community within the intestine was assessed by the denatur-
ing gradient gel electrophoresis (DGGE) of partial 16S rRNA. No lesions were observed in the
intestinal epithelia; however, the presence of NPs in diets changed the structure of the intestinal
microbial community. Some beneficial bacterial strains (e.g.,
Cetobacterium somerae
) were sup-
pressed to nondetectable levels by Cu-NPs exposure, and two unidentified bacterial clones from
the
Firmicutes phylum
were sensitive to Cu, but were present in Ag-treated and control fish. In
zebrafish, unique microbiome changes caused by the exposure to Ag- and Cu-NPs indicate that
the ingestion of NPs could affect the function of the digestive system and the organism's health
(Daniel et al. 2013).
13.5.6 t
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adMIuM
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Wang et al. evaluated the possible toxicity due to the exposure of cadmium-selenium quantum dots
(CdSe QDs) via ingestion on enterocyte-like Caco-2 cells as a small intestine epithelial model. Cells
were incubated in Cd
+2
(2-200 nmol/mL) containing a medium for 24 h. A Cd
+2
concentration of
200 nmol/mL resulted in a drop of the relative viability of Caco-2 to 0.62, which is considerably
lower than the control. However, cytotoxicity largely depended on the coating and treatment of
QDs (e.g., acid treatment and dialysis). This concluded that Caco-2 cell viability correlated with the
concentration of free Cd
+2
ions present in cell culture medium. CdSe QDs exposure to low gastric
pH affected cytotoxicity, indicating that the route of exposure may be an important factor in QDs
cytotoxicity (Wang et al. 2008b).
13.5.7 t
oxIcIty
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I
aNd
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o p
artIcles
The GI route represents the most common and patient-compliant route of drug administration.
However, some drugs have poor pharmacokinetic profiles when administered orally (Bimbo et al.
2011). The major barriers in oral delivery are the enzymes in the upper parts of the GI system,
the pH changes in the GI tract, the absorption and efficient permeability across the intestinal wall
(Ramesan and Sharma 2009), the presence of bile salts (Qian and Bogner 2012), and liver-mediated,
first-pass metabolism (Bimbo et al. 2011). pH levels change throughout the GI tract: The pH in the
stomach is 1-3, while in the small intestine, the pH is 6.5-7.0 and in the colon, it is 7.0-8.0 (Cheng
et al. 2011). Drug absorption occurs through paracellular transport along the epithelial lumen of
the small intestine. However, the tight junctions among adjacent enterocytes form a barrier for
drugs (Foraker et al. 2003). The presence of bile salts can affect the structure of the drug molecule
and, therefore, its function. The absorbed drugs then pass through entero-hepatic circulation and
the active agent is cleared by the “first-pass metabolism” in the liver before reaching systemic
circulation and the intended site.
