Objective To study the antagonism of DMSO against the toxicity of cooking oil fume condensation to BEAS-2B cell.Methods The comet assay,micronucleus test and multinucleated cells test were used to research the genotoxicity induced by cooking oil fume condensation(COFC)and the antagonism of DMSO.Results COFC induced DNA broken,the tail area,rate of comet occurrence,tail length,tail moment,olive tailmoment increased significantly,the frequencies of micronucleus and multinucleated cells were significantly increased and the damage of cells could be inhibited effectively by DMSO.Conclusion The antagonistic effects of DMSO on the toxicity of COFC was significant in BEAS-2B cell.

Objective To observe the effect of S-band micro-wave long-term intermittent irradiation on endocrine function in rats.Methods A total of 192 rats (male and female) were randomly divided into the sham-irradiation (normal control) groups and the irradiation groups.The irradiation groups were exposed with micro-wave at 3 dosages of 4,10 and 20 mW/cm2 for 6 min twice a week for 12 weeks,while no administration was given to control group.The endocrine parameters in blood serum were examined by radioimmunoassay at 4,8,12 week during irradiation and 4 week post-irradiation.Results After the irradiation of S-band microwave,parts of the endocrine parameters changed.T3 in famale rats decreased at first and then increased,especially in 10 mW/cm2 group at 8 and 12 week,20 mW/cm2 group at 4 and 12week(t =-2.586,-2.642,-5.075,-4.365,P <0.05).FT3 in famale rats had the similar trend asT3,significantly lower in 4 and 10 mW/cm2 groups than that in the control group at 4 week (t = 2.275,2.510,P <0.05),then increased,especially in three irradiation groups at 12 week (t =-2.636,-2.851,-5.240,P < 0.05).TSH decreased at 4 week,especially in 10 mW/cm2 group (t = 2.300,P < 0.05) ; and then increased in the irradiation groups at 20 mW/cm2 at 8 and 12 week (t =-2.838,-3.651,P <0.05).COR and ACTH in male rats showed changes in volatility,in which the 4,10 and 20 mW/cm2 groups at 8 week increased significantly (t =-2.772,-2.234,-2.505,P < 0.05),while 20 mW/cm2 group at 12 week decreased significantly (t=3.067,P < 0.05).E2 in female rats was slightly lower in irradiation groups at 4 week than the control group,then increased,especially in 10 mW/cm2 group at 8 week,three irradiation groups at 12 week (t =-2.322,-3.179,-2.655,-4.716,P < 0.05),and returned to the normal at 4 week post-irradiation,significantly lower in 4 mW/cm2 group than that in the control group (t = 2.250,P < 0.05).T in male rats increased first and then decreased,especially in 10 mW/cm2 group at 8 week(t =-2.435,P < 0.05).After exposure the above indexes restored to some extent.Conclusions The long-term intermittent irradiation of S-band microwave can cause adverse effects on the endocrine function of rats.

Objective: To study the effects of nano red elemental selenium on liver protection, tumor inhibition and immune regulation. [WT5FZ]Methods: [WT5BZ]Models of acute liver injury induced by CCl 4, S 180 tumor growth and immune regulation were used. Results: Nano red elemental selenium could increase blood and liver Se contents, inhibit the increase of liver MDA and serum AST induced by CCl 4, decrease tumor weight and increase phagocytic ratio and NK cell activity in S 180 bearing mice, increase immune activities in normal mice. All these improvements were statistically significant (P

Objective To investigate the phagocytosis function of cigarette smoke extracts (CSE)on the NR8383 cells. Methods The concentration of CSE and the optimal time was defined by cell counting kit-8 assay, Annexin V/PI cell apoptosis assay and CFSE cell proliferation assay. The cell was gained after exposed to the different concentration of CSE for 24 h and mixed with fluorescein-labeled Escherichia coli in 37℃ for 2 h. The fluorescence intensity was used to assay the phagocytosis function of NR8383 cells.Results The phagocytosis function of NR8383 cells may be changed by the concentration of CSE. In the concentration of 100 μg/ml, the phagocytosis function of NR8383 was enhanced 0.5 times than the normal cell when NR8383 cell was exposed to CSE, and the specific activity is the highest. When NR8383 cells were exposed to CSE and LPS, the phagocytosis function of NR8383 cells was enhanced 2 times than the normal cell. In the concentration of 200 μg/ml, the phagocytosis function of NR8383 cells was damaged, the rate of apoptosis is the 54. 1%. Conclusion Low concentration of CSE enhanced the phagocytosis function of NR8383 cells, but high concentration of CSE damaged the phagocytosis function of NR8383 cells. This study reveals a new role of CSE as an activator of macrophage function.

A novel suspension array technology was established for the detection of three kinds of veterinary drug residues: chloramphenicol, clenbuterol and 17-β-estradiol. The three conjugates in which veterinary drugs coupled with BSA were immobilized on the solid carrier of the suspension microarray-polystyrene fluorescent microspheres/beads as detective probes. Indirect competitive technology was employed. Competitive reactions between the veterinary drugs in the aqueous phase and the veterinary drugs-BSA conjugates on the beads for coupling with their complimentary specific biotinylated monoclonal antibodies were carried out. And then, straptavidin-phycoerythrin was added for coupling and the fluorescent signals were captured. Afterwards the detective standard curves were plotted. The regular ELISA standard curves of the three veterinary drugs were also plotted. Comparison between suspension array and regular enzymE-linked immunosorbent assay(ELISA) was in the respects of the detective technology, the detection limits, the detective ranges, the samples detection and the multi-analysis. Suspension array technology is distinct advantageous except for specificity. There was well consistent performance between the two methods. The high-throughput suspension array provides a novel method for multi-analysis of veterinary drugs with simple operation, sensitive, rapid and low costing.

Objective To observe the oxidative damage in human bronchial epithelial cells(BEAS-2B) induced by depleted uranium(DU)and protection of DMSO.Methods The measurement of extracellular superoxide anions(O2-·)was based on the reduction of ferricytochrome C.Quantitative analysis of extracellular hydrogen peroxides(H2O2)was used by the horseradish peroxidase-dependent oxidation of phenol red.The determination of extracellular hydroxyl radicals(·OH)was based on discoloration of safranine T.Ethidium bromide and 2,7'-dichlorofluorescein,fluorescent products of the membrane-permeable dyes-hydroethineand 2,7'-dichloroflurescin diacetate were used to monitor the intracellular production of O2-·and H2O2 by fluorometric method.The enzyme activity of SOD and GSH were measured by chemiluminescence and spectrophotometric method,respectively.Results The ROS production,including H2O2,O2-·and·OH,increased remarkably which induced by DU in BEAs-2B cells.The enzyme activity of SOD and GSH was descended remarkedly.These changes could be effectively inhibited by 0.5% of DMSO.Conclusions DU causes oxidative damage to BEAS-2B cells.Through removing active oxygen,DMSO can inhibit oxidative damage of DU.

Objective To investigate the distribution of uranium in rats after inhalation with depleted uranium aerosols. Methods The depleted uranium aerosols were inhaled by Wistar rats. At 30, 90, 180, 270, 360, and 540 d after inhalation, the rata were sacrificed and tissue samples were collected. The contents of uranium in lung, kidney, liver, heart, brain, thighbone, spleen and thymus were measured by laser time-dependent spectroscopy analysis. Resulits The uranium contents of lung increased in the high-dosc and low-dose groups [(499833.3 ± 14214.8) ng/g and (25 424.0 ± 6193.4)ng/g, respectively] after inhalation, and significantly differed from the control (28.8 ± 13.9)ng/g, (P < 0.05).At 30 d after inhalation, the contents of uranium in lung, kidney and thighbone were higher than those of control, and then decreased time-dependently. At 60 d, the contents of uranium in liver, heart, brain, spleen and thymus were higher than those of control. Curve of the eontenta were biphasie, whieh went up first, reached at peak value and then went down. The contents of uranium were high in lung, thighbone, brain and thymus. Conclusions After inhalation of depleted uranium aerosols, lung and thighbone are the primary reservoirs for uranium redistributed, and accumulations in brain and thymus suggest other two organs for unanticipated injury by depleted uranium.

Objective To investigate the effect of citric acid and ambroxol on clearing insoluble particles of depleted uranium in rat lungs by establishing a tracheal perfusion model.Methods One hundred and fifty male Wistar rats were randomly divided into model exposure group, normal control group(NC group), depleted uranium exposure group(DU), citric acid treatment group( CA) , ambroxol treatment group( AM) and citric acid+ambroxol treatment group( CA+AM) . The rats were sacrificed on 7, 15 and 30 days.Uranium content in the lungs was detected by microwave digestion method, pathological changes in the lungs were observed, and inflammatory factors of lung homogenates were detected.Results Compared to DU control group, the intrapulmonary uranium deposit amount in experimental groups was significantly reduced on 7 and 15 days (P<0.05).HE stained lung tissue showed that the pathological changes in treatment groups were less significant than in DU control group.The level of IL-1α,IL-1β,and IL-2 was significantly lower than in DU control, but the level of MCP-1 and MIP-1 was observably higher.Conclusion Citric acid and ambroxol can evidently improve the clear-ance of lung uranium and reduce damnification of lung tissues.Drug treatment can reduce the level of pulmonary inflamma-tory cytokines alleviate the chronic inflammation in the lungs, and enhance the capacity of macrophage to recruitment.

AIM: To investigate the role of transcription factor hairy and enhancer of split 1 (Hes1) in the malignant transformation of human bronchial epithelial cell line BEP2D induced by tobacco.METHODS: The BEP2D cells were chronically exposed to cigarette smoke condensate (CSC) at 1 cigarette per L until the 70th generation.The phenotype of malignant transformation of the cells induced by CSC was detected by soft agar clony formation assay.RT-PCR and Western blot were used to determined the expression of Hes1 at mRNA and protein levels in each generation of the cells.The proliferation and apoptosis of the BEP2D cells exposed to CSC were analyzed with the methods of MTT assay, flow cytometry and cell colony formation assay after treatment with Notch pathway bloker DAPT or liposome transfection with Hes1-siRNA.The expression of Hes1 in the peripheral small airway tissues of the smoking rats was evaluated by immunohistochemical staining.The expression of Hes1 in non-small-cell lung cancer and normal airway tissues was also detected by the methods of immunohistochemistry and RT-PCR.RESULTS: The BEP2D cells in the 70th generation had a malignant transformation phenotype.The expression of Hes1 in the BEP2D cells exposed to CSC for different time showed an increa-sing trend.DAPT and liposome transfection with Hes1-siRNA down-regulated the expression of Hes1, inhibited the cell proliferation and induced cell apoptosis.The expression of Hes1 in the airway mucosa of the rats exposed to cigarette smoke for 1 month and 6 months was significantly higher than that in control group.Cigarette smoking induced the expression of Hes1 in lung cancer and normal airway tissues.CONCLUSION: Hes1 may be involved in smoking-induced lung cancer by promoting the imbalance between apoptosis and proliferation.

Objective To construct the recombinant eukaryotic expression plasmids of human adenylyl cyclase-associated protein 1 (CAP1)and to explore its intracellular location and functions.Methods By using Hela cDNA as the template,the cDNAs encoding CAP1 was amplified by PCR and inserted into pCMV-Myc vector to construct the recombinant plasmid.The recombinant plasmid was transfected into 293 cells using lipofectamine 2000.The protein expression and the intracellular location of the inserted gene were confirmed by Western blotting and immunofluorescence,respectively.Scratch-repair experiment was used to detect the cancer cells’ migration ability.Results The recombinant eukaryotic expression plasmid of human CAP1 was successfully constructed and transfected into eukaryote cells.The recombinant plasmid was successfully expressed in eukaryote cells.CAP1 was located in the cytoplasm.The results of scratch-repair experiment showed that the overexpression of CAP1 could significantly inhibit the cells’ migration.Conclusion CAP1 recombinant plasmid was successfully expressed in eukaryotic cells.CAP1 protein was located in the cytoplasm.The overexpression of CAP1 inhibited cell migration. The present study provides important experimental evidence for further study on CAP1.