Disease relevance of methanesulfonic acid

• This study attempted to characterize proteins cross-linked to DNA of Yoshida lymphosarcoma cells treated with methylene dimethanesulfonate (MDMS) and its hydrolytic products formaldehyde (HCHO) and methanesulfonic acid (MSA) [1].
• The importance of hydrophobicity in the mutagenicity of methanesulfonic acid esters with Salmonella typhimurium TA100 [2].
• It was shown that DNA lesions, leading to GC-->AT transitions, induced by MMS in vivo are not repaired in adapted E. coli cells [3].
• On the other hand, Zn pretreatment was not accompanied by resistance against MMS toxicity [4].
• To investigate their role in cellular defense against genotoxic compounds, we comparatively analysed chromosomal aberrations and apoptosis induced by ultraviolet (UV-C) light and the potent alkylating agent methyl methanesulfonate (MMS) in primary diploid mouse fibroblasts knockout for either c-Fos or p53, or double knockout for both genes [5].

High impact information on methanesulfonic acid

• These studies indicate that mitochondrial or nuclear targeting of MGMT protects hematopoietic cells against cell killing by BCNU, TMZ, and MMS, which is consistent with the possibility that mitochondrial DNA damage and nuclear DNA damage contribute equally to alkylating agent-induced cell killing during chemotherapy [6].
• The formation of S-3-sulfopropylcysteine in proteins and the subsequent hydrolysis of the proteins with methanesulfonic acid are particularly useful for complete amino acid analysis at the picomole level using a single sample [7].
• The key intermediate for these syntheses, 12-methoxy-DB[a,l]P, was successfully obtained by cyclization of 6-(3-methoxybenzyl)benzanthrone with methanesulfonic acid, which in turn was prepared by 1,4 conjugate addition of 3-methoxybenzyl magnesium bromide to benzanthrone [8].
• Esterification of taxol using N,N-dialkylated amino acids gave 2'-amino acid esters of taxol, 2'-(N,N-dimethylglycyl)taxol (4) and 2'-[3-(N,N-diethylamino)propionyl]taxol as its methanesulfonic acid salt (5b), in good yield [9].
• 8-Amino-3-deazaguanine, as its methanesulfonic acid (mesylate 7), exhibited an inhibition constant (IC50) of 9.9 microM against isolated mammalian PNP [10].

Chemical compound and disease context of methanesulfonic acid

• We examined DMP 728 [(cyclic[D-2-amino-butyryl-N2-methyl-L-arginyl-glycyl-L-aspartyl-3-(a min o- methyl-benzoic acid], methanesulfonic acid salt], a cyclic peptidomimetic, GPIIb/IIIa receptor antagonist, for prevention of thrombosis and rethrombosis in a canine model of carotid artery thrombosis [11].
• Administration of 1-10 nmol/l SM-20550 [N-(aminoiminomethyl)-1,4-dimethyl-1H-indole-2-carboxamide methanesulfonic acid] before and after ischemia prevented impairment of acetylcholine-induced relaxation [12].
• Chemotherapeutic management of bronchogenic carcinoma: trials with NSC-140117, a new methanesulfonic acid ester of aminoglycol [13].

Biological context of methanesulfonic acid

• Twelve mutants with increased sensitivity to MMS and one mutant with increased sensitivity to histidine showed Mendelian segregation of the mutant phenotypes [14].
• The close association of these putative transport genes to the MSAMO structural genes msmABCD suggested a role for these genes in transport of methanesulfonic acid (MSA) into M. methylovora. msmEFGH and msmABCD constituted two operons for the coordinated expression of MSAMO and the MSA transporter systems [15].
• For MMS and ENU we followed cultures for several days, and found that WI-L2-NS cells underwent delayed apoptosis 3 to 5 days after treatment, in parallel with published observations with ionizing radiation [16].
• The results of this in vivo study showed that TA had no suppressing effect on chromosome loss occurring spontaneously or after induction by MMS in mature spermatozoa [17].
• The observed difference between MMS and MNU when combined with GEN would not have been predicted on the basis of a simplistic interpretation of DNA methylation as the mode of action and may be due to differences in the profile of DNA methylations and/or epigenetic effects [18].

Anatomical context of methanesulfonic acid

• The data indicate that MMS and MNNG-induced cell death in mouse fibroblasts is triggered by the activation of the mitochondrial damage pathway and that apaf-1 is required for eliciting this response [19].
• The SS breaks induced by MMS and 4NQO were largely repaired by HeLa cells during a 5-h post-treatment incubation [20].

Associations of methanesulfonic acid with other chemical compounds

• A simple method of replica plating has been used to isolate mutants of Neurospora crassa that have increased sensitivity to methyl methanesulfonate (MMS) and/or to histidine [14].
• In this procedure, samples are hydrolyzed with methanesulfonic acid (MSA) in order to avoid the conversion of MetSO to methionine (Met) that occurs during hydrolysis of protein in HCl [21].
• The tryptophan content of purified bovine rhodopsin was obtained by two independent methods: direct analysis of hydrolysates prepared by digestion of opsin with methanesulfonic acid containing 0.2% 3-(2-aminoethyl)indole and a computer-assisted analysis of the near-UV spectrum of rhodopsin [22].
• The FPC cells that showed hyper-sensitivity to 4NQO were also hyper-sensitive to mitomycin C (MMC), but susceptibilities of these cells to UV radiation, methyl methanesulfonate (MMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were within the normal range [23].
• These data on MNNG and MMS in vitro were in fair agreement with the directions of mutation in vivo [24].

Gene context of methanesulfonic acid

• Sensitivity of dap1 strains to MMS is not due to loss of damage checkpoints [25].
• The N-terminal region of Sgs1, which interacts with Top3, is required for complementation of MMS sensitivity and suppression of hyper-recombination in sgs1 disruptants [26].
• Cleavage does not occur during necrosis or following exposure to H(2)O(2) or methanesulfonic acid methyl ester. p140 is unlikely to be able to functionally replace p261 in vivo, since it does not bind to PCNA or the other pol epsilon subunits [27].
• Marinosulfonomonas methylotropha strain TR3 is a marine methylotroph that uses methanesulfonic acid (MSA) as a sole carbon and energy source [28].
• Colony forming efficiency was measured for APC, MMS and ENU, and was greater in the p53 mutant cells [16].

Analytical, diagnostic and therapeutic context of methanesulfonic acid

• EM dihydrate was prepared by three methods, one of which included suspending the anhydrous drug in an aqueous solution of 1.0 M methanesulfonic acid to form a slurry, followed by filtration [29].
• Amino acid analysis by high-performance liquid chromatography with methanesulfonic acid hydrolysis and 9-fluorenylmethylchloroformate derivatization [30].
• Alkylsulfonates from methanesulfonic acid to decanesulfonic acid were separated by isotachophoresis with conductivity detection in a common electrolyte system at pH 4 [31].
• HPLC analysis of fatty acyl-glycine in the aqueous methanesulfonic acid hydrolysates of N-terminally fatty acylated peptides [32].
• The effects of SM-20550 [N-(aminoiminomethyl)-1,4-dimethyl-1H-indole-2-carboxamide methanesulfonic acid], an Na+/H+ exchange inhibitor, on ischemic preconditioning (IPC) were studied in a rabbit model of myocardial ischemia and reperfusion injury [33].

References