Eugenol attenuates TiOnanoparticles-induced oxidative damage, biochemical toxicity and DNA damage in Wistar rats: an in vivo study.
Environ Sci Pollut Res Int. 2021 Jan 9. Epub 2021 Jan 9. PMID: 33420693
Mohammad Rafiq Wani
Titanium dioxide nanoparticles (TiONPs) are widely used in food, edible dyes, and other commercial products. Human exposure to TiONPs has raised concerns regarding their toxic potential. Various studies have evaluated the TiONPs-induced toxicity, oxidative damage to the cellular components, and genotoxicity. In the present study, we examined whether co-treatment with the dietary antioxidant eugenol can attenuate or protect against TiONPs-induced toxicity. We exposed the adult male Wistar rats to TiONPs (150 mg/kg body weight) by intraperitoneal injection (i.p.) either alone or as co-treatment with eugenol (1-10 mg/kg body weight) once a day for 14 days. The untreated rats were supplied saline and served as control. Titanium (Ti) accumulation in various tissues was analyzed by inductively coupled plasma mass spectrometry. Serum levels of liver and kidney biomarkers and oxidative stress markers in the liver, kidney, and spleen were determined. A significant increase in hydrogen peroxide level confirmed that oxidative stress occurred in these tissues. TiONPs induced oxidation of lipids, and decreased glutathione level and antioxidant enzyme activity in the kidney, liver, and spleen of treated rats. TiONPs also increased the serum levels of alanine aminotransferase, alkaline phosphatase, aspartate aminotransferase, albumin, and total cholesterol and decreased the blood urea nitrogen, uric acid, and total bilirubin in serum, which indicates oxidative damage to the liver and kidney. In eugenol and TiONPs co-treated rats, all these changes were mitigated. Single-cell gel electrophoresis (comet assay) of lymphocytes showed longer comet tail length in TiONPs-treated groups, indicating DNA damage while tail length was reduced in eugenol and TiONPs co-treated groups. Thus, it seems that eugenol can be used as a chemoprotective agent against TiONPs-induced toxicity.