C-reactive Protein Signaling and Chromosomal Abnormalities in Nanotoxicity Induced via Different Doses of TiO2 (80nm) Boost Liver Function.

Abstract

The wide application of nanotechnology merits the need to clarify their nanotoxicity. In vivo studies have raised concerns about the toxicity of titanium dioxide nanoparticles (TiO2 NPs), but there are limited data on chromosomal abnormalities induced in hepatic tissue. In this article, the toxicity of three IP doses of TiO2 NPs (80nm) (50, 250, and 500mg/kg) through three time intervals (up to 7, 15, and 45days) on liver tissue was assessed. Hepatic catalase (CAT), glutathione (GSH), nitric oxide (NOx), and malondialdehyde (MDA) levels varied with the administered dose and exposure time of TiO2 NPs. As a result, TiO2 NPs caused a statistically significant decrease in hepatic CAT and GSH activities and a significant alleviation in MDA and NOx levels (p < 0.05), suggesting that the liver exposed to these various doses of TiO2 NPs suffered from severe oxidative stress. The extent of depletion of antioxidant enzymes and the elevation of MDA and NOx in the liver exposed to the highest dose and duration of TiO2 NPs 500mg for 45days was the greatest, suggesting that the toxicity might be dose and time dependent. Further, C-reactive protein (CRP) as an inflammatory marker was also alleviated, in addition to the apparent chromosomal aberration and liver pathologies including necrotic and fibrotic hepatocytes after exposure to 250 and 500mg/kg of TiO2 NPs for 14 and 45days that were deduced. Hence, nanotechnology-based industries are growing rapidly leading to large-scale production of engineered nanoparticles. They contribute to increased chances of human NPs exposure and health risk.