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The Silicon Dioxide NPs showed an insignificant increase of 3.4% tail DNA at 100 mg/ml (p > 0.05). The highest % tail DNA was observed in Co3O4 NPs and the least % tail DNA was observed in Al2O3 NPs. The Al2O3 NPs showed an insignificant increase of 2.8% tail DNA at 100 mg/ml (p > 0.05). When compared with control, an insignificant increase (p >0.05) in chromosomal aberrations was observed when exposed to SiO2 and Al2O3 NPs (p > 0.05). The Co3O4 NPs (p < 0.001) and Fe2O3 NPs (p < 0.05) showed a significant increase in chromosomal aberration when compared with control at 100 mg/ml. A minimum of 50 metaphases per sample were scored for the chromosome aberration assay.

The surface charge and ionic strength are the main reasons for agglomeration of theSilicon Dioxide NPs in the lymphocyte culture medium. The addition of FBS has effects on the stability of Al2O3 NPs. The lymphocyte culture medium contains amino acids, vitamins, and salts that cause decrease in electrostatic repulsive forces and increase in ionic strength forming NPs aggregation. The serum contains proteins that prevent the aggregation of the NPs by creating a protein corona. The agglomeration of NPs was lower at 10% FBS than the serum-free media. The agglomeration of NPs was less in 10% FBS than the serum-free media. 

When exposed to Silicon Dioxide NPs, the excessive ROS can cause injuries and impair the function of lymphocytes by aggravating the effect of LPO and damaging the intracellular components of a cell completely including its proteins, lipids, and DNA . Oxidative stress and alteration in the level of antioxidant enzymes observed with alumina NPs are mainly due to the pro-inflammatory effects through ROSmediated mechanism. The oxidative stress disturbs the cellular macromolecules such as lipids, proteins, and DNA when exposed to NPs. The DNA damage occurs mainly due to mutations, deletions, cross-linking, and formation of adducts leading to apoptosis. The caspases play a significant role in the initiation and execution of apoptosis causing cellular DNA damage by Co3O4 NPs in human lymphocytes. The Fe2O3 NPs cause chromosomal DNA fragmentation and nuclear condensation in human lymphocytes. The Fe2O3 NPs arrest the G0/G1 phase in a dose-dependent manner.



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