4.1 Article

Effect of low-dose exposure of aluminium oxide nanoparticles in Swiss albino mice: Histopathological changes and oxidative damage

Journal

TOXICOLOGY AND INDUSTRIAL HEALTH
Volume 36, Issue 8, Pages 567-579

Publisher

SAGE PUBLICATIONS INC
DOI: 10.1177/0748233720936828

Keywords

Aluminium oxide nanoparticles; DNA damage; hepatocellular; histopathology; neurodegeneration; ROS

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Rapid growth in the use of aluminium oxide nanoparticles (Al(2)O(3)NPs) in various fields such as medicine, pharmacy, cosmetic industries, and engineering creates concerns since the literature is replete with data regarding their toxicity in living organisms. The objective of the present study was to demonstrate the potential toxicological manifestations of repeated exposure to Al2O3NP at low dosesin vivo. In the present study, Al2O3NP was orally administered at 15, 30 or 60 mg kg(-1)body weight for 5 days to Swiss albino male mice. A battery of well-defined assays was undertaken to evaluate aluminium (Al) bioaccumulation, haematological and histological changes, oxidative damage and genotoxicity. Physico-chemical characterisation demonstrated increases in hydrodynamic diameter along the concentration gradient of Al2O3NP dispersed in MilliQ water. Brain, liver, spleen, kidney and testes showed high Al retention levels. Histopathological lesions were prominent in the brain and liver. Al2O3NP treatment increased levels of lipid peroxidation and decreased glutathione content in the test organs at all dose levels. The enzyme activities of catalase and superoxide dismutase were also significantly altered. DNA damage quantified using the comet assay was markedly increased in all the soft organs studied. Anatomical abnormalities, redox imbalance and DNA damage were positively correlated with Al retention in the respective organs. Size, zeta potential and colloidal state might have contributed to the bio-physico-chemical interactions of the NPsin vivoand were responsible for the non-linear dose response. The overall data indicate that Al2O3NP exposure may result in adverse health consequences, inclusive of but not limited to disturbed redox homeostasis, hepatocellular toxicity, neurodegeneration and DNA damage.

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