ABSTRACT
Objective@#To investigate the expression and role of LINC00052 during glycidyl methacrylate (GMA) -induced malignant transformation of 16HBE cells.@*Methods@#Human bronchial epithelial (16HBE) cells were divided into GMA transformation group and corresponding DMSO control group, and the 10th, 20th and 30th generation cells of each group were collected LncRNA microarrays were used to analysis expression of LINC00052 in different stage of malignant transformation. Bioinformatics analysis was applied and the relative expression of LINC00052 and its potentially target genes was detected by real-time quantification PCR (qPCR) .@*Results@#The results of microarray analysis showed that LINC00052 was up-regulated by 1.32-fold, down-regulated by 1.64-fold and down-regulated by 4.92-fold in the malignant transformation early (P10) , middle term (P20) and late (P30) , respectively, The results of qPCR showed that compared with the DMSO control group, the expression of LINC00052 was up-regulated by 1.55 times, down-regulated by 1.20 times and down-regulated by 2.35 times in P10, P20 and P30, respectively, and the difference was statistically significant (P<0.05) . There was a statistically significant difference in the relative expression of NTRK3 between the GMA transformation group of P10 and P30 generations with the corresponding DMSO control group (P<0.05) .@*Conclusion@#LINC00052 is highly expressed in early time of GMA-induced malignant transformation of 16HBE, and down-regulated in the middle and last stage of malignant transformation and may play a protective role in GMA-induced malignant transformation of 16HBE by influencing the expression of its target gene NTRK3.
ABSTRACT
Objective@#To investigate Oxidative damage effects induced by CdTe Quantum Dots (QDs) in mice.@*Methods@#40 ICR mice were randomly divided into 5 groups: one control group (normal saline) ; four CdTe QDs (exposed by intravenous injection of 0.2 ml of CdTe QDs at the concentration of 0、0.5、5.0、50.0 and 500.0 nmol/ml respectively) . After 24 h, the mice were decapitated and the blood was collected for serum biochemically indexes、hematology indexes, the activities of SOD、GSH-Px and the concentration of MDA were all detected.@*Results@#The results showed in the four CdTe QDs exposure groups, the level of CRE、PLT and the concentration of MDA were all significantly lower than those of the control group (P<0.05 or P<0.01) ; the activities GSH-Px in 50.0 and 500.0 nmol/ml CdTe QDs group were significantly higher than those of control group (P<0.01) .@*Conclusion@#It was suggested that CdTe QDs at 0.5 nmol/ml could induce Oxidative damage effects in mice.
ABSTRACT
<p><b>OBJECTIVE</b>To analyze the opioid binding protein/cell adhesion molecule-like (OPCML) methylation status at different stages of malignant transformation of human bronchial epithelial (16HBE) cells induced by Glycidyl Methacrylate (GMA) and to explore the effect of OPCML methylation in the process of malignant transformation.</p><p><b>METHODS</b>Cells were harvested at different stages (the 10th generation, the 20th generation and the 30th generation). To verify the Methylation chip result of OPCML methylation status in the process of malignant transformation, we detected it by methylation-specific-PCR (MSP); Real-time fluorescence Quantitative PCR (qPCR) were applied to measure the gene expression levels of OPCML at different transformed stage, and compared with the control groups (treated with DMSO).</p><p><b>RESULTS</b>Based on the result of methylation chip, the gene of OPCML methylation occurred in all stages, which was consistent to the result of MSP; qPCR showed that the levels of gene expression decreased in the 20th generation and 30th generation.</p><p><b>CONCLUSION</b>Methylation status of OPCML gene promoter could be considered as a stable and specific biomarker in the transformation process.</p>
Subject(s)
Humans , Cell Adhesion Molecules , Metabolism , Cell Transformation, Neoplastic , Cells, Cultured , DNA Methylation , Epithelial Cells , Cell Biology , Epoxy Compounds , GPI-Linked Proteins , Metabolism , Genes, Tumor Suppressor , Methacrylates , Promoter Regions, GeneticABSTRACT
<p><b>OBJECTIVE</b>To develop a method for determination of 2, 4-dichlorophenoxyacetic acid (2, 4-D) in the air of workplace by high-performance liquid chromatography.</p><p><b>METHODS</b>2, 4-D was collected by ultrafine glass filters, desorbed by methanol, separated by a C18 column, and detected by a UV detector. Identification and quantification of 2, 4-D were performed by retention time and peak areas, respectively.</p><p><b>RESULTS</b>The linear range of the test was 2∼200 µg/ml; the elution efficiency was 94.6%- 95.9%; the limit of detection (S/N = 3) was 0.034 µg/ml (injection volume of 20 µl eluant); the lower limit of quantification (S/N = 10) was 0.11 µg/ml; the minimum detectable concentration was 0.011 mg/m(3); the minimum quantifiable concentration was 0.037 mg/m(3) (with sampled air volume of 45 L).</p><p><b>CONCLUSION</b>This method is convenient and simple in sample collection and preparation, and satisfies all methodological requirements. Therefore, this method is useful for the determination of 2, 4-D in the air of workplace.</p>
Subject(s)
2,4-Dichlorophenoxyacetic Acid , Air , Air Pollutants, Occupational , Chromatography, High Pressure Liquid , Methods , WorkplaceABSTRACT
<p><b>OBJECTIVE</b>To investigate the polymorphism of delta-aminolevulinic acid dehydratase(ALAD) and the genetic susceptibility to lead toxicity in Uighur and Yi population in China.</p><p><b>METHODS</b>The ALAD genotypes were determined by PCR and MspI restriction fragment length polymorphism techniques in 214 Uighur individuals from Xinjiang autonomous region and 144 Yi individuals from Yunnan province. The correlation between the polymorphism of ALAD and blood lead levels, and the factors affecting the latter were explored.</p><p><b>RESULTS</b>The frequencies of the allele ALAD1 and ALAD2 in Uighur are 0.91 and 0.09; and in Yi are 0.98 and 0.02 respectively. In Uighur the average blood lead level was (76 +/- 4) microgram/L, and 25.7% individuals with blood lead level > or = 100 micrograms/L. In Yi the average blood lead level was (50 +/- 16) microgram/L, and 6.3% individuals with blood lead level > or = 100 micrograms/L. However, no statistic correlation between the distribution of ALAD alleles and the blood lead level was found in both populations.</p><p><b>CONCLUSION</b>The genetic susceptibility of ALAD polymorphism to lead toxicity may exhibit in a lead dose-dependent manner.</p>