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. 2018 May 26;6(2):29.
doi: 10.3390/toxics6020029.

Zinc Oxide Nanoparticles Induced Oxidative DNA Damage, Inflammation and Apoptosis in Rat's Brain after Oral Exposure

Hala Attia  1   2 , Howaida Nounou  3 , Manal Shalaby  4
Affiliations

Zinc Oxide Nanoparticles Induced Oxidative DNA Damage, Inflammation and Apoptosis in Rat's Brain after Oral Exposure

Hala Attia et al. Toxics. .

Abstract

Growing evidences demonstrated that zinc oxide nanoparticles (ZnONPs) could reach the brain after oral ingestion; however, the "neurotoxicity of" ZnONPs after oral exposure has not been fully investigated. This study aimed to explore the "neurotoxicity of" ZnONPs (.

Keywords: DNA fragmentation; Fas; ZnONPs; brain; caspase-3; heat shock protein-70; interleukin-1β; oxidative stress.

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Conflict of interest statement

The authors declare they have no competing interests.

Figures

Figure 1
Figure 1
The brain levels of oxidative stress markers in normal control and different ZnONPs-treated groups. Data are expressed as mean ± SEM. a: significantly different from normal control; b: significantly different from G I; c: Significantly different from G II; d: Significantly different from G III. * p < 0.05; ** p < 0.01; *** p < 0.001. MDA: Malondialdehyde (the index of lipid peroxidation), GSH: Reduced glutathione (a non-enzymatic antioxidant), SOD: superoxide dismutase; CAT: Catalase (enzymatic antioxidants). G I & G II: rats treated with 40 and 100 mg/kg for 24 h, respectively. G III & G IV are rats treated with 40 and 100 mg/kg/day for 7 days, respectively.
Figure 2
Figure 2
The brain levels of nitrite (an index of nitric oxide production) in normal control and different ZnONPs-treated groups. Data are expressed as mean ± SEM. a: significantly different from normal control; * p < 0.05; ** p < 0.01. G I & G II: rats treated with 40 and 100 mg/kg for 24 h, respectively. G III & G IV are rats treated with 40 and 100 mg/kg/day for 7 days, respectively.
Figure 3
Figure 3
The brain levels of the inflammatory markers in normal control and different ZnONPs-treated groups. Data are expressed as mean ± SEM. a: Significantly different from normal control; b: Significantly different from G I; c: significantly different from G II. ** p < 0.01; *** p < 0.001. TNF-α: tumor necrosis factor-α; IL-1β: interleukin-1β. G I & G II: Rats treated with 40 and 100 mg/kg for 24 h, respectively. G III & G IV are rats treated with 40 and 100 mg/kg/day for 7 days, respectively.
Figure 4
Figure 4
The brain levels of heat shock protein-70 (HSP-70) and DNA fragmentation in normal control and different ZnONPs-treated groups. Data are expressed as mean ± SEM. a: Significantly different from normal control; b: significantly different from G I; c: significantly different from G II; d: Significantly different from G III. * p < 0.05; ** p < 0.01; ***p < 0.001. G I & G II: rats treated with 40 and 100 mg/kg for 24 h, respectively. G III & G IV are rats treated with 40 and 100 mg/kg/day for 7 days, respectively.
Figure 5
Figure 5
Comet DNA assay in brain tissues. G I & G II: rats treated with 40 and 100 mg/kg for 24 h, respectively. G III & G IV are rats treated with 40 and 100 mg/kg/day for 7 days, respectively.
Figure 6
Figure 6
The brain levels of apoptotic markers (caspase-3 and Fas) in normal control and different ZnONPs-treated groups. Data are expressed as mean ± SEM. a: significantly different from normal control; b: significantly different from G I; c: significantly different from G II. * p < 0.05; ** p < 0.01; *** p < 0.001. G I & G II: rats treated with 40 and 100 mg/kg for 24 h, respectively. G III & G IV are rats treated with 40 and 100 mg/kg/day for 7 days, respectively.
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