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1.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 405-408, 2013.
Article in Chinese | WPRIM | ID: wpr-343663

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the role of ubiquitin ligase Ring2 in the DNA damage induced by benzo[a]pyrene (B[a]P).</p><p><b>METHODS</b>The expression of Ring2 in human bronchial epithelial (16HBE) cells was inhibited by small interfering RNA (siRNA) to obtain siRNA-Ring2 16HBE cells. The siRNA-Ring2 16HBE cells, as well as normal 16HBE cells, were exposed to B[a]P (0, 1, 2, 4, 8, 16, and 32 µmol/L) for 24 h; other siRNA-Ring2 16HBE cells and normal 16HBE cells were exposed to B [a]P (16 µmol/L) for 0, 1, 2, 4, 8, 12, and 24 h. The levels of DNA damage were evaluated by alkaline single cell gel electrophoresis assay.</p><p><b>RESULTS</b>After being treated with siRNA for 36 h, the siRNA-Ring2 16HBE cells showed a 72% decrease in Ring2 expression compared with normal 16HBE cells. The analysis of covariance showed that whether to be treated with siRNA and concentration of B[a]P had impacts on Olive tail moment (OTM) (P = 0.032 and P < 0.001); the adjusted mean of OTM was significantly higher in siRNA-Ring2 16HBE cells than in normal 16HBE cells. Whether to be treated with siRNA and B[a]P exposure time had impacts on OTM (P = 0.031 and P < 0.001); the adjusted mean of OTM was significantly higher in siRNA-Ring2 16HBE cells than in normal 16HBE cells.</p><p><b>CONCLUSION</b>The DNA of 16HBE cells with decreased Ring2 expression has increased susceptibility to B[a]P, which may be due to reduced H2A monoubiquitination following decrease in Ring2 expression.</p>


Subject(s)
Humans , Benzo(a)pyrene , Toxicity , Bronchi , Cell Biology , Cell Line , DNA Damage , Epithelial Cells , Metabolism , RNA, Small Interfering , Tumor Suppressor Proteins , Genetics , Metabolism , Ubiquitin Thiolesterase , Genetics , Metabolism
2.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 434-436, 2011.
Article in Chinese | WPRIM | ID: wpr-272573

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the brain oxidative stress injury induced by nano-alumina particles in ICR mice.</p><p><b>METHODS</b>Sixty male ICR mice were randomly divided into 6 groups: control group, solvent control group, 100 mg/kg micro-alumina particles group, 3 groups exposed to nano-alumina particles at the doses of 50, 100 and 200 mg/kg. The mice were exposed by nasal drip for 30 days. Then levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-PX) in brain tissues of mice were detected.</p><p><b>RESULTS</b>There was no difference of SOD activity in mouse brain between control group [(17.32 +/- 6.23)U/gHb] and 50 mg/kg nano-alumina particles group [(17.89 +/- 1.82) U/gHb]. The SOD activity [(4.93 +/- 2.30)U/gHb] in 200 mg/kg nano-alumina particles group was significantly lower than that in control group (P < 0.05). The MDA levels in 3 nano-alumina particles groups were (0.76 +/- 0.13), (1.00 +/- 0.30) and (1.16 +/- 0.39)nmol/ml, respectively, which were significantly higher than that [( 0.24 +/- 0.09)nmol/ml] in control group (P < 0.05). The GSH levels in 3 nano-alumina particles groups were (0.72 +/- 0.08), (0.55 +/- 0.19) and (0.61 +/- 0.20)mg/gpro, respectively, which were significantly lower than that [(1.55 +/- 0.34)mg/gpro]] in control group (P < 0.05). The CAT activity in 50 and 100 mg/kg nano-alumina particles groups were (10.40 +/- 3.84) and (10.40 +/- 2.00)U/mgpro, respectively, which were significantly higher than that [(5.79 +/- 0.96) U/mgpro] in control group (P < 0.05). The CAT activity [(3.25 +/- 1.04)U/mgpro] in 200 mg/kg nano-alumina particles group was significantly lower than that in control group (P < 0.05 ).</p><p><b>CONCLUSION</b>Nano-alumina particles can induce the oxidative stress damage in brain tissues of mice.</p>


Subject(s)
Animals , Male , Mice , Aluminum Oxide , Toxicity , Cerebral Cortex , Metabolism , Glutathione Peroxidase , Metabolism , Malondialdehyde , Metabolism , Mice, Inbred ICR , Nanoparticles , Toxicity , Oxidative Stress , Superoxide Dismutase , Metabolism
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