RESUMO
A new composite electrode (G-PSE) was developed from graphite powder and expanded polystyrene (EPS, Styrofoam) by simply dissolving the foam in chloroform, incorporating the graphite particles under mixing and volatilizing the solvent at 80 °C. The resulting rigid black composite can be softened with acetone and so it can easily be molded to any shape, e.g., into a PTFE tube with an electric contact, to build the electrode. A 75% graphite content (w/w) was found appropriate for preparing the G-PSE with a working potential similar to that of carbon paste electrodes, superior mechanical stability and a much faster response to ferrocyanide, close to reversible and similar to that of the much more expensive glassy carbon electrode. Applications of the G-PSE to dipyrone and paracetamol quantification in pharmaceutical formulations were demonstrated. The results accomplished by flow injection analysis with amperometric detection at the G-PSE were successfully validated against standards methods.
RESUMO
Azidothymidine (AZT) is an antiretroviral drug that affects cell proliferation, apoptosis, and the NF-κB pathway. As multiple myeloma (MM) presents with constitutive activation of NF-κB, we analyzed the effect of AZT on human MM cell lines. We evaluated the cytotoxic effect of AZT in human MM cell lines sensitive (8226/S) or resistant to doxorubicin (8226/DX5) and human T cell lymphoblast-like cells, uterine sarcoma cells, and HUVEC using MTT assay. Cytotoxicity was also evaluated in vivo in nude mice xenografted with 8226/S tumor. The effect of AZT on the expression of genes involved in cell proliferation, apoptosis, angiogenesis, and the NF-κB pathway was analyzed in the xenografts using real-time polymerase chain reaction. AZT was effective against both 8226/S and 8226/DX5 cells in a dose and time-dependent manner (p = 0.02) in vitro and promoted cell cycle arrest in S phase in these cells. The tumor volume was lower in mice treated with AZT compared to untreated mice (p = 0.0003). AZT down-regulated the pro-proliferative genes encoding AKT1, MYC, STAT1, MAPK8, MAPK9, CCL-3, Bcl-3, and cyclin D2; pro-angiogenenic genes encoding VEGF and IL8; and genes involved in cell adhesion (ICAM1 and FN1) and the NF-κB pathway. AZT up-regulated the expression of tumor suppressor gene FOXP1 and the pro-apoptotic genes encoding BID, Bcl-10, and caspase-8. Thus, we demonstrated the cytotoxic effect of AZT in human MM cell lines for the first time. Our data may provide the rationale for future clinical trials of AZT for treating MM.
