فهرست مطالب dr majid mahdiyeh

Nitric oxide (NO) has signaling property in plants، therefore the effect of nitroprusside (SNP) as an NO producing agent on viability in the cell culture، lipid peroxidation and activity of superoxide dismutase، catalase and peroxidase in the callus of Catharantus roseus was investigated. Cell suspension was prepared from callus of Catharantus roseus، and the cells were treated with 0، 10، 50، 100، 150، 200 and 250 μM of sodium nitroprusside for 1، 3 and 6 days to determined the cell viability (based on trypan blue staining as well as MTT colorimetric assay). Then using 100 and 200 mM of sodium nitroprusside as selected dose، the cell suspension was used to investigate the cell morphological changes. In addition the callus tissue was treated with the same dose to estimate the level of lipid peroxidation and the activity of superoxide dismutase، catalase and guaiacol peroxidase. Comparison of the data from trypan blue and MTT methods showed that the significant (p<0. 05) differences in viability was concentration dependent with respect to control. Base on the morphology، SNP caused changes in the shape and size of the cell nuclei as well as disturbance in the chromatin. In addition changes in the cytoplasm such as shrinkage and cell border deform was observed in the treated cells compare to control. Also activity of the investigated enzymes following the oxidative stress increased significantly (p<0. 05). The level of malondialdehyde as an indicator of lipid peroxidation also increased significantly. Sodium nitroprusside as an NO producing agent caused cellular membrane damage which results in cell viability reduction in the callus of catharantus roseus. Although the activity of the antioxidant enzymes increased significantly with respect to the oxidative stress but the produced cellular response was not able to compensate the damages.

Environmental contaminants such as bisphenol A, in addition to the environmental problems can affect human health. Epigallocatechingallat has been found to have antioxidant and cytoprotective properties in cultured cells but its effect on toxicity induced by bisphenol A has not yet been determined in mesenchymal stem cells. The aim of this investigation was to study the protective role of epigallocatechingallat in rat bone marrow mesenchymal stem cells following treatment with bisphenol A(an oxidative stress inducer). In this experimental study, rat bone marrow mesenchymal stem cells were extracted using flashing-out method and cultured in DMEM containing 15% FBS and 100U/ml Pen/Strep. At the end of the third passage, cells were divided into 4 groups: control, bisphenol A, bisphenol A + epigallocatechingallat and epigallocatechingallat. The groups were treated for 12, 24, 36, and 48 hrs. After treatment with bisphenol A and epigallocatechingallat, viability, morphology, rate of DNA damage and calcium content of the cells were evaluated. Data were analyzed by one way ANOVA. p<0.05 was considered significant. Bisphenol A caused a significant reduction in the viability and calcium content of the cells. In addition, morphological changes such as nuclear breakage and chromatin condensation, as well as cytoplasm shrinkage, were observed in the group treated with bisphenol A. We found alterations in these parameters in the group of bisphenol A+ epigallocatechingallat which were similar to those observed in the control ones. Epigallocatechingallat can produce a protective role against the toxic effects of bisphenol A in the mesenchymal stem cells.