Abstract:
TiO2 NPs are used in many fields such as food industry, medicine and agriculture. Despite the advantages of nanotechnology, the adverse effects of nanoparticles are inescapable. The current study was designed to assess the protective impact of vitamin E (VE) on the nephrotoxicity of TiO2 NPs at the histological and molecular level. Mice were randomly divided into 4 groups: G 1, control without any treatment; G 2, vitamin E (100 mg/kg/day); G 3, mice exposed to TiO2NPs (1499 mg/kg/day) for 5 consecutive days ; G4, TiO2-NPs+VE daily. Histologically, TiO2-exposed animals revealed highly-destructed renal parenchyma with ruptured glomerular elements, apoptotic nuclei, inflammatory leucocytic infiltration, damaged distal convoluted tubules containing proteinaceous material in its lumens, highly distorted glomeruli and focal necrosis. Molecularly, TiO2 NPs-intoxicated animals resulted in a marked increase in DNA fragmentation for 2.4 folds in tail DNA (2.404 %) and 4.9 folds in tail moment DNA (7.093) as compared to control. Co-administration of vitamin E to TiO2 NPs-intoxicated mice partially protected their renal tissue from DNA damage as indicated by a marked decrease in tail DNA (2.049%) and tail moment (5.347) as compared to that given TiO2 NPs only. However, VE co-treatment with TiO2 nanoparticles partially-returned the renal tissue to the normal histological structure and minimized DNA damage, where a mild degree of cellular repair in the renal parenchyma could be detected. We can conclude that VE supplementation may play a promising role in reducing the nephrotoxicity of TiO2 NPs in experimental animals at the level of applied doses.