Stability of the glycosidic bond of S-adenosylsulfonium compounds toward acid

Schlenk, F.; Zydek-Cwick, Cynthia R.

doi:10.1016/0003-9861(69)90301-4

Cited by 37 publications

(11 citation statements)

References 21 publications

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“…radio-activity 50-60 Ci/mol) was purchased from New England Nuclear Corp., Boston, MA, U.S.A. Decarboxylated S-adenosylmethionine, both unlabelled and labelled in the methyl group, was prepared by the action of S-adenosylmethionine decarboxylase from Escherichia coli and purified as described by Pos6 et al (1976). Labelled 5'-methylthioadenosine was prepared from the S-adenosyl-L-[methyl-14C]methionine by heating at 900C in 0.25M-sodium citrate, pH4, for 45min and purified by chromatography on Dowex 50 (H+ form; Schlenk & Zydek-Cwick, 1969). All other biochemicals were obtained from the Sigma Chemical Co., St. Louis, MO, U.S.A.…”

Section: Methodsmentioning

confidence: 99%

Effects of inhibitors of spermidine and spermine synthesis on polyamine concentrations and growth of transformed mouse fibroblasts

Pegg

Borchardt

Coward

1981

Biochemical Journal

103

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1. A number of compounds known to inhibit polyamine biosynthesis at various steps in the biosynthetic pathway were tested for their ability to inhibit growth and decrease polyamine concentrations in virally transformed mouse fibroblasts (SV-3T3 cells). 2. Virtually complete inhibition of growth was produced by the inhibitors of ornithine decarboxylase alpha-methylornithine and alpha-difluoromethylornithine and by the inhibitors of S-adenosylmethionine decarboxylase 1,1'-[(methylethanediylidene)dinitrilo]diguanidine and 1,1'-[(methylethanediylidene)dinitrilo]bis-(3-aminoguanidine). The former inhibitors decreased putrescine and spermidine contents in the cells to very low values, whereas the latter substantially increased putrescine but decreased spermidine concentrations. The inhibitory effects of all of these inhibitors on cell growth could be prevented by the addition of spermidine, suggesting that spermidine depletion is the underlying cause of their inhibition of growth. 3. alpha-Difluoromethylornithine, which is an irreversible inhibitor of ornithine decarboxylase, was a more potent inhibitor of growth and polyamine production (depleting spermidine almost completely and spermine significantly) than alpha-methylornithine, which is a competitive inhibitor. This was not the case with the inhibitors of S-adenosylmethionine decarboxylase where 1,1'-[(methylethanediylidene)dinitrilo]diguanidine, a reversible inhibitor, was more active than 1,1'-[(methylethanediylidene)dinitrilo]bis-(3-aminoguanidine), an irreversible inhibitor. It is suggested that this effect may be due to the lesser uptake and/or greater chemical reactivity of the latter compound. 4. Various nucleoside derivatives of S-adenosylhomocysteine that inhibited spermidine synthase in vitro did not have significant inhibitory action against polyamine accumulation in the cell. These compounds, which included S-adenosylhomocysteine sulphone, decarboxylated S-adenosylhomocysteine sulphone, decarboxylated S-adenosylhomocysteine sulphoxide and S-adenosyl-4-thio-butyric acid sulphone did not inhibit cell growth or polyamine content until cytotoxic concentrations were added. 5. 5'-Methylthioadenosine, 5'-isobutylthioadenosine and 5'-methylthiotubercidin, which inhibit aminopropyltransferase activity in vitro, all inhibited cell growth and decreased spermidine content. Although these compounds were most active against spermine synthase in vitro, they acted in the cell primarily to decrease spermidine content. Cell growth could not be restored to normal values by addition of spermidine, suggesting that these nucleosides have another inhibitory action towards cellular proliferation. 6. 5'-Methylthioadenosine and 5'-isobutylthioadenosine are degraded by a phosphorylase present in SV3T3 cells, yielding 5-methylthioribose-1-phosphate and 5-isobutylthioribose-1-phosphate respectively, and adenine. This degradation appears to decrease the inhibitory action towards cell growth, suggesting that the nucleosides themselves are exerting the inhibitory action. 5'-Methylthio...

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Section: Methodsmentioning

confidence: 99%

Effects of inhibitors of spermidine and spermine synthesis on polyamine concentrations and growth of transformed mouse fibroblasts

Pegg

Borchardt

Coward

1981

Biochemical Journal

103

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“…The lack of 5'-methylthioadenosine phosphorylase has been confirmed in our present strains of these cells. We have prepared radiolabeled 5'-methylthi0[~H]Ado from [3H]5'-adenosylmethionine according to established procedures [33] and have shown that it is not metabolized by either P388-M or L1210 cells (data not shown). The alternative, therefore, was contamination of the P388-M cells by mycoplasma, which is known to possess Ado phosphorylase activity In a previous study [2] we failed to detect mycoplasma in P388-M cultures by the Urd/Ura incorporation method [16].…”

Section: Resultsmentioning

confidence: 99%

Mycoplasma contamination alters 2′‐deoxyadenosine metabolism in deoxycoformycin‐treated mouse leukemia cells

Plagemann

Woffendin

1990

J of Cellular Biochemistry

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Deoxycoformycin-treated P388 and L1210 mouse leukemia cells salvage 2'-deoxyadenosine from the medium only inefficiently, because deoxyadenosine deamination is blocked and its phosphorylation is limited by feedback controls. Mycoplasma contamination at a level that had no significant effect on the growth of the cells increased the salvage of deoxyadenosine greater than 10 fold over a 90 min period of incubation at 37 degrees C, but in this case deoxyadenosine was mainly incorporated into ribonucleotides and RNA via adenine formed from deoxyadenosine by mycoplasma adenosine phosphorylase. Deoxyadenosine was an efficient substrate for this enzyme, in contrast to 2',3'-dideoxyadenosine which was not phosphorolyzed. Mycoplasma infection was confirmed by the presence of uracil phosphoribosyltransferase activity and by culture isolation. The contaminant has been identified as Mycoplasma orale. Mycoplasma infection had no effect on the deamination and phosphorylation of deoxyadenosine and adenosine, on the salvage of hypoxanthine and adenine, or on the degradation of dAMP and dATP by the cells or on their acid and alkaline phosphatase activities.

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“…Unlabeled SAM and SAH were obtained from Boehringer Mannheim Corp. MTA was the product of Sigma Chemical Co. S-Adenosyl-D-methionine was prepared by the methylation of S-adenosyl-D-homocysteine (22); the latter was synthesized from D-homocysteine by the procedure of Sakami (11). 5'-Dimethylsulfonium adenosine (DMTA) was prepared from MTA by treatment with methyl iodide (9,14…”

Section: Methodsmentioning

confidence: 99%

Inhibition of leucine transport in Saccharomyces by S-adenosylmethionine

Law¹,

Ferro²

1980

J Bacteriol

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S-Adenosyl-L-methionine (SAM) inhibited leucine transport in Saccharomyces cerevisiae. By using a mutant defective in the active transport of SAM, we demonstrated that the inhibitory effect was exerted at an extracellular site. Cells preincubated with SAM for 120 min became refractory to its inhibitory effect, which was not a result of either the active transport or the metabolism of SAM. The quantitative recovery of labeled SAM from the incubation medium indicated that SAM, and not a metabolite, was the true inhibitory molecule. S-Adenosyl-L-homocysteine and S-adenosyl-L-ethionine also functioned as inhibitors of leucine transport, whereas S-adenosyl-D-methionine, S-adenosyl-D-homocysteine, 5'methylthioadenosine, 5'-dimethylthioadenosine, and adenosine lacked this property. Kinetic studies demonstrated that SAM was a competitive inhibitor of leucine transport.Portions (0.2 ml) were centrifuged at low speed, and 427 on August 1, 2020 by guest

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Stability of the glycosidic bond of S-adenosylsulfonium compounds toward acid

Cited by 37 publications

References 21 publications

Effects of inhibitors of spermidine and spermine synthesis on polyamine concentrations and growth of transformed mouse fibroblasts

Effects of inhibitors of spermidine and spermine synthesis on polyamine concentrations and growth of transformed mouse fibroblasts

Mycoplasma contamination alters 2′‐deoxyadenosine metabolism in deoxycoformycin‐treated mouse leukemia cells

Inhibition of leucine transport in Saccharomyces by S-adenosylmethionine

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