ABSTRACT
<p><b>OBJECTIVE</b>To investigate the expression variation of RAR-β2, RASSF1A, and CDKN2A gene in the process of nickel-induced carcinogenesis.</p><p><b>METHODS</b>Nickel subsulfide (Ni(3)S(2)) at dose of 10 mg was given to Wistar rats by intramuscular injection. The mRNA expression of the three genes in induced tumors and their lung metastasis were examined by Real-time PCR. The methylation status of the 5' region of these genes were detected by Quantitative Real-time methylation specific PCR.</p><p><b>RESULTS</b>The mRNA expressions of the three genes both in muscle and lung tumor were decreased distinctly in comparison with normal tissue. But hypermethylation was found only in muscle tumor.</p><p><b>CONCLUSION</b>These findings suggest that loss of function or decrease of RAR-β2, RASSF1A, and CDKN2A, as well as the hypermethylation of 5' region of these genes, are related with nickel exposure.</p>
Subject(s)
Animals , Male , Rats , Carcinogens , Toxicity , CpG Islands , Cyclin-Dependent Kinase Inhibitor p16 , Genetics , Metabolism , DNA Methylation , Gene Expression Regulation, Neoplastic , Lung Neoplasms , Metabolism , Muscle Neoplasms , Metabolism , Nickel , Toxicity , Rats, Wistar , Receptors, Retinoic Acid , Genetics , Metabolism , Tumor Suppressor Proteins , Genetics , MetabolismABSTRACT
OBJECTIVE: To analyze the characteristics of adverse drug reaction (ADR) induced by Levofloxacin (LVFX) injection and to promote rational use of drugs in the clinic. METHODS: 137 LVFX injection-induced ADR cases reported in our hospital during 2006～2009 were collected and analyzed statistically with Excel in respect of age, gender, medication and clinical manifestation, etc. RESULTS: ADR cases occurred nearly in all ages of people, and 32.85% were appeared in people over 60 years. Main clinical manifestations were lesion of skin and its appedants (62.04%) and gastrointestinal injury (16.06%). Most of them were mild and medium ADR. CONCLUSION: Great importance should be attached to the rational use of LVFX injection and ADR monitoring to guarantee the safety of patients.
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Objective:To study the effects of vitamin C (VC) on the injury of alveolar macrophages exposed to Ni2O3 in vitro and the expression of inducible nitric oxide synthase (iNOS). Method:The alveolar macrophages were cultured with exposure to Ni2O3 in vitro. Meanwhile,VC with different concentrations (25,50 and 100 ?mol/L) were added to the medium, respectively. The cell activity,nitric oxide(NO),reactive oxygen species (ROS), malondialdehyde (MDA) and activities of SOD, GSH-Px,CAT and iNOS were detected. iNOS mRNA expression was detected by using RT-PCR. Results:VC could decrease mortality and increase survival activity of alveolar macrophages. VC could also decrease ROS,NO and NOS activity,increase SOD,GSH-Px, CAT activities and downregulate the expression of iNOS mRNA. Conclusion:The lipid peroxidation of alveolar macrophage could be induced by Ni2O3. VC could downregulate the expression of iNOS mRNA and reduce the production of ROS and NO through increasing the activity of antioxidative enzymes and antagonize the oxidative damage induced by Ni2O3.
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Objective To observe the DNA damage in the human lung fibroblasts(HLF)induced by insoluble nickel compounds(Ni3S2 and Ni2O3)and soluble nickel compound(NiSO4),and to study the mechanism of carcinogenesis.Methods The DNA damage of HLF cells treated with different concentrations of Ni3S2,Ni2O3 and NiSO4 were detected with the method of single cell gel electrophoresis(SCGE).Results All of the three kinds of nickel compounds significantly caused DNA damage in HLF cells,the average tail moments of all nickel-treated groups were larger than those in the control group(P
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Objective To investigate the changes of ultrastructure and Bax,Bcl-2 expression of cerebral cortex in lymphostatic encephalopathy(LE).Methods LE models were established by occluding and removing both the shallow and deep cervical lymph nodes in rats.Ultrastructural changes of the cerebral cortex were observed at 1 d,2 d,3 d,5 d,7 d and 14 d after operation.Expression of Bax and Bcl-2 were examined by Western blot.Results Brain edema appeared under electron microscope in LE model group.The perivascular spaces in the cortex were enlarged and full of fluid,the dropsical nerve fibers had swelling and fragmented myelin sheath.Some neurons showed apoptotic conformation and some had characters of necrosis.The changes mentioned above were the most serious at day 5.The protein expression of Bax,Bcl-2 and the ratios of Bax/Bcl-2 in LE 3 d,5 d,7 d groups were significantly higher than those in normal control group(all P
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Objective: To study the effects of vitamin E and selenium on apoptosis and c-Myc expression in human leukemia cells. Methods: DNA gel electrophoresis and Northern blotting hybridization were used to detect the apoptosis and the expression of c-Myc gene, respectively. Human leukemia cell line HL-60 and K562 were cultured in vitro. Results: The apoptosis of HL-60 and K562 cells were induced after being exposed to vitamin E (100 ?mol/L) and selenium (8 ?mol/L) for 24 hours, respectively. In HL-60 cell line, c-Myc mRNA was down-regulated significantly by vitamin E(100 ?mol/L),but not selenium(8 ?mol/L).In contrast, the expression of c-Myc gene was repressed by selenium(8 ?mol/L) and not by vitamin E(100 ?mol/L) in K562 cell. Conclusion: Our observations suggest that c-Myc down-regulation and induction of apoptosis by selenium and vitamin E are important pathways in repressing leukemia cell proliferation.The results suggest there are different mechanisms of repressing leukemia cell proliferation for selenium and vitamin E.