Background: Titanium dioxide (TiO2) nanoparticles are
among the largely manmade nanomaterials
worldwide and are broadly used as both industrial and user products.
The primary target site for several nanoparticles is the liver, including
TiO2 nanoparticles (TNPs), exposed directly or indirectly
through ingestion of contaminated water, food, or animals and elevated
environmental contamination. Oxidative stress is a known facet of
nanoparticle-induced toxicity, including TNPs. Mitochondria are potential
targets for nanoparticles in several types of toxicity, such as hepatotoxicity.
Nevertheless, its causal mechanism is still controversial due to scarcity
of literature linking the role of mitochondria-mediated TNP-induced
hepatotoxicity. Aim: The objective of
the current study was to evaluate the relation of mitochondrial oxidative
stress and respiratory chain mechanisms with TNP-induced mitochondrial
dysfunction in vitro, and explore the hepatoprotective
effect of quercetin (QR), which is a polyphenolic flavonoid abundant
in fruits and vegetables with known antioxidant properties, on TNP-induced
mitochondrial oxidative stress and disturbance in respiratory chain
complex enzymes in the liver of rats. Results: Enzymatic
and non-enzymatic antioxidant levels, oxidative stress markers, and
mitochondrial complexes were assessed with regard to TNP-induced hepatotoxicity.
The depleted lipid peroxidation levels and protein carbonyl content,
in mitochondria, induced by TNPs were restored significantly by pretreatment
with QR. QR modulated the altered non-enzymatic and enzymatic antioxidants
and mitochondrial complex enzymes. Conclusion: Based on the findings, we conclude that QR, which mitigates
oxidative stress caused by mitochondrial dysfunction, holds promising
capability to potentially diminish TNP-induced adverse effects in
the liver.