Sulfasalazine in vitro

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Cancer Treat Rep ; Interaction studies with fruit extracts in the Ussing chamber system, as well as in the in-situ intestinal perfusion study, revealed a 2- to 4-fold increase in the absorptive transport of sulfasalazine. Our research focused on a specific growth and viability requirement of lymphoid cells. Sulphasalazine inhibits macrophage activation: However, there is evidence that gem can cause reactive oxygen intermediates roi s in pancreatic cancer cells At the highest sulfasalazine concentration of 5 m mthere were 8- and 3-fold reductions in IL-6 release and and 6-fold reductions in IL-8 release from adipose tissue and skeletal muscle, respectively.

Elimination of such roi s by glutathione could contribute to the drug resistance of the cells.

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It also plays an important role as a detoxifier and is known to underlie drug resistance 45. Growth inhibition resulting from glutathione depletion has been observed in a variety of experimental systems, including those involving pancreatic cancer 23 and glioma 10 cells, and can be overcome by inclusion in the culture medium of glutathione ethyl ester, a membrane-permeable form of glutathione Cell Immunol ; The marked suppression by sulfasalazine of rat Nb2 pre-T cell lymphoma growth in vivo without major toxicity to the host Figure 5together with its efficacy against human DoHH2 B-cell lymphoma cells in vitro Figure 2asuggest that sulfasalazine has potential application in clinical treatment of cancers dependent on extracellular cyst e ine for growth and viability.

Thus sulfasalazine-induced loss of cell viability started after about 48 hours of incubation [ Figure 2 B ], at a time when glutathione levels had been severely reduced for at least 24 hours [ Figure 1 B ]. No major side effects were observed in vivo. Animal care and experiments were carried out in accordance with the guidelines of the Canadian Council on Animal Care.

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In this study, its intestinal transport characteristics were studied in an in-vitro, ex-vivo and in-situ system. Culture growth inhibitions were calculated from the cell number increases found at hour 45 in drug-treated cultures and their controls.

Sensitization of pancreatic cancer cells by sulfasalazine has also been reported by other researchers.

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Supplemental Content Full text links. With regard to sodium salicylate, it may be noted that its lymphoma growth-inhibitory activity was apparently not based on inhibition of cyclooxygenase COX-1 activity. Intracellular depletion of glutathione, a major free-radical scavenger, has been associated with growth arrest and reduced drug resistance chemosensitization of cancer cells. Intracellular depletion of glutathione, a major free-radical scavenger, has been associated with growth arrest and reduced drug resistance chemosensitization of cancer cells.

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Its inhibition could lead to cyst e ine deficiency in lymphoma cells via reduction of both their cystine uptake and cysteine supply by somatic cells. It appears therefore that the suppression of Nb2-U17 lymphoma growth by sulfasalazine Figure 5 was not due to a direct drug - tumor cell interaction, but involved an indirect effect of the drug.

Expression of the x c - cystine transporter in cell lines. Pharmacological and biochemical actions of sulphasalazine.

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Adipose tissue tumour necrosis factor and interleukin-6 expression in human obesity and insulin resistance.

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