Detail of "5072-26-4"

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Reduction in cellular glutathione by buthionine sulfoximine and sensitization of murine tumor cells resistant to L-phenylalanine mustard

Reduction in cellular glutathione by buthionine sulfoximine and sensitization of murine tumor cells resistant to L-phenylalanine mustard. Somfai-Relle, Susan; Suzukake, Kayoko; Vistica, Barbara P.; Vistica, David T. (Lab. Med. Chem. Pharmacol., Natl. Cancer Inst., Bethesda, MD 20205, USA). Biochem. Pharmacol. 5072-26-4 and 148-82-3 which are cas registry numbers are also used here., 33(3), 485-90 (English) 1984. CODEN: BCPCA6. ISSN: 0006-2952. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The sensitization of the resistant tumor cell to L-phenylalanine mustard (L-PAM) [148-82-3] by decreasing cellular glutathione [70-18-8] was reversible and was influenced by the availability of L-cysteine [52-90-4]. Also, DL-buthionine-S,R-sulfoximine (I) [5072-26-4], an inhibitor of glutathione formation, was capable of sensitizing murine L-1210 cells resistant to L-PAM. Sensitization of the resistant tumor cells to L-PAM occurred at inhibitor concns. that were minimally cytotoxic, required a sufficient exposure time to the inhibitor to decrease the cellular content of glutathione prior to treatment with L-PAM, and occurred in the presence of amino acid precursors utilized for glutathione biosynthesis. In vivo studies suggest that sustained administration of I resulted in sensitization of resistant tumor cells within the peritoneal cavity to L-PAM. The failure to observe significant increases in the lifespan of these animals is due to metastatic invasion and growth of the tumor in host organ, notably the liver. .

Nonprotein thiols and the radiation response of A549 human lung carcinoma cells

Nonprotein thiols and the radiation response of A549 human lung carcinoma cells. Biaglow, John E.; Clark, Edward P.; Epp, Edward R.; Morse-Guadio, Michele; Varnes, Marie E.; Mitchell, James B. (Dep. Radiol., Case Western Reserve Univ., Cleveland, OH 44106, USA). Int. J. Radiat. Biol. Relat. Stud. Phys., Chem. Med., 44(5), 489-95 (English) 1983. CODEN: IJRBA3. ISSN: 0020-7616. DOCUMENT TYPE: Journal CA Section: 8 (Radiation Biochemistry) Glutathione (GSH)-depletion by butionine sulfoximine (BSO) altered both the aerobic and anaerobic radiation response of A549 human lung cancer cells grown in vitro. The O enhancement ration (OER) was increased slightly from 3.0 to 3.3. The lack of an effect of GSH-depletion on OER redn., provides a system whereby the mechanism of action of the thiol-reactive reagent di-Et maleate (DEM) can be investigated. Pretreatment of cells with DEM, under nontoxic concns., removed 13% of the intracellular nonprotein thiols (NPSH) and resulted in an OER of 2. When BSO followed by DEM was used, so that both GSH and NPSH were reduced to 0, an OER of 1.5 was obtained. Cells treated with 1 mM BSO for 24 h contained 10% NPSH and no GSH. When these cells were exposed to 0.5 or 1 mM DEM briefly, during irradn., the OER was 2.4 and 1.7, resp. In some cases, altered OER occurred in combination with increased aerobic responses. 5072-26-4 and 70-18-8 which are cas registry numbers of substances are two of reagents here. This was esp. true for aerobic irradiations of BSO-treated cells in the presence or absence of DEM. However, the increased aerobic response was offset by a more increase in the hypoxic response. These results indicate (1) that GSH plays a significant role in aerobic radiation response but is not a principal factor in OER redn., and (2) that redn. of the OER by DEM is not due primarily to GSH removal. The preferential radiosensitization of hypoxic cells by DEM may involve reactions of this compd. with NPSH or protein SH, or may be related to the ability of DEM to mimic O as a hypoxic cell radiosensitizer. .