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Titanium Dioxide Nanoparticles Trigger Loss of Hepatic Function and Perturbation of Mitochondrial Dy
閱讀：261 發(fā)布時(shí)間：2015-6-2| 提 供 商 | 美國(guó)布魯克海文儀器公司 | 資料大小 | 2.1MB |
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Titanium dioxide (TiO2) nanoparticles are one of the most highly manufactured
nanomaterials in the world with applications in copious industrial and consumer products.
The liver is a major accumulation site for many nanoparticles, including TiO2, directly
through intentional ingestion or indirectly through increased environmental contamination
and unintentional ingestion via water, food or animals. Growing concerns over the current
usage of TiO2 coupled with the lack of mechanistic understanding of its potential health
risk is the motivation for this study. Here we determined the toxic effect of three different
TiO2 nanoparticles (commercially available rutile, anatase and P25) on primary rat
hepatocytes. Specifically, we evaluated events related to hepatic functions and
mitochondrial dynamics: (1) urea and albumin synthesis using colorimetric and ELISA
assays, respectively; (2) redox signaling mechanisms by measuring ROS production; (3)
OPA1 and Mfn-1 expression that mediates the mitochondria dynamics by PCR; and (4)
mitochondrial morphology by MitoTracker Green FM staining. All three TiO2
nanoparticles induced a significant loss in hepatic functions even at concentrations as low
as 20 μg/ml with commercially used P25 causing maximum damage. TiO2 nanoparticles
induced a strong oxidative stress in primary hepatocytes.TiO2 nanoparticles exposure also
resulted in morphological changes in mitochondria and significant loss in the fusion
process, thus impairing the mitochondrial dynamics. Although this study demonstrated that
TiO2 nanoparticles exposure resulted in significant damage in primary hepatocytes, more
in vitro and in vivo studies are required to determine the complete toxicological mechanism
on primary hepatocytes and subsequently liver function.