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