Disease relevance of methylbenzene

• The suppressive effect on the bone resorption was not affected by treatment of caldecrin with phenylmethyl sulfonyl fluoride or by use of protease-deficient mutant caldecrins [1].
• A series of carbamimidothioic acid phenylmethyl ester salts and their N,N'-tetramethyl derivatives were synthesized, many of which exert an interesting inhibiting action on Gram-positive and Gram-negative bacteria and also on fungi [2].

High impact information on methylbenzene

• Here, we report that phenethyl isothiocyanate and other structurally related isothiocyanates, phenylmethyl isothiocyanate, phenylbutyl isothiocyanate, and phenylhexyl isothiocyanate, but not phenyl isothiocyanate induced apoptosis in HeLa cells in a time- and dose-dependent manner [3].
• The rate constant for hydrogen atom abstraction at 298 K by benzyl radical from 1 is 2 orders of magnitude greater than that from 1-octanethiol, resulting from the predicted (DFT) S-H bond strength of 1 of 73 kcal/mol [4].
• Analyses were carried out in both uncoated and phenylmethyl-coated capillaries of fused silica with internal diameters of 50 and 100 microns, respectively, and an effective column length of 50 cm [5].
• Proteolytic inhibitors, such as phenylmethyl sulfonyl fluoride and pancreatic trypsin inhibitor, caused partial inhibition of the activity responsible for the conversion of S to F, whereas inhibitors of peroxidase activity had no effect [6].
• The same INC involving a complex between the benzyl radical and protonated carbon dioxide is also generated upon decarboxylation of metastable phenylacetic acid molecular ions [7].

Biological context of methylbenzene

• It was found that alpha-ammonium, alpha-phosphonium, and alpha-sulfonium groups all destabilize a methyl radical. alpha-Ammonium also destabilizes a benzyl radical, whereas alpha-phosphonium and alpha-sulfonium either slightly stabilize or destabilize a benzyl radical depending on their alkylation state [8].
• When hydrolysis of anandamide was inhibited by an amidase inhibitor (phenylmethyl sulfonyl fluoride; PMSF), however, SR141716A significantly attenuated anandamide's effects but did not completely block them [9].

Anatomical context of methylbenzene

• The enzyme could be released from microsomes by Triton X-100 treatment and the solubilised enzyme was found to be inhibited by puromycin and sulphydryl reagents but to be unaffected by phosphoramidon, captopril, phenylmethyl sulphonyl fluoride and by chelating agents except 1,10-phenanthroline [10].
• Inactivated trypsin, i.e. phenylmethyl sulfonyl-trypsin or soybean trypsin inhibitor treated trypsin, was not able to activate latent human leukocyte collagenase [11].
• Contrary to the suggestion that inactive proteases activate latent human polymorphonuclear leukocyte collagenase, the inactive phenylmethyl sulfonyl-trypsin could not activate latent collagenase [12].
• The level of receptors remained stable for 12 months when stored at -70 degrees C with the inclusion of 10 mM phenylmethyl sulfonyl-fluoride in the cytosol extraction buffer [13].
• Human leucocyte response to migration inhibitory activity from lymphocytes. Modification by aprotinin, Tranexamic acid and phenylmethyl sulfonylfluoride [14].

Associations of methylbenzene with other chemical compounds

• DPP IV activity was inhibited by diisopropylfluorophosphate and phenylmethyl sulphonylfluoride [15].
• The proteinase was not inhibited by phenylmethyl sulfonyl fluoride but was inhibited by o-phenanthroline and ethylenediaminetetraacetic acid [16].
• To make this point more clear, the fluorescence spectra of the benzyl radical and its deuterated compounds in methylcyclohexane (MCH) have been observed at 4.2 K and detailed vibrational analysis has been carried out [17].
• The effects of the activators trypsin, phenylmercuric chloride, phenylmethyl sulfonyltrypsin, and N-ethylmaleimide on the latent human polymorphonuclear leukocyte collagenase were studied [12].
• When VRR-12, preincubated with bivalent antiserum against Saw-scaled and Russell's viper venom or EDTA was injected, haemorrhagic activity was not reduced, on the other hand preincubation with phenylmethyl sulphonyl fluoride reduced the activity markedly [18].

Gene context of methylbenzene

• The reactions of Fe(III)(TPA) (TPA = tris(2-pyridylmethyl)amine) complexes with 2-methyl-1-phenyl-2-propyl-hydroperoxide (MPPH) delivered by syringe pump under anaerobic conditions afford nearly quantitative conversion of MPPH to products derived from the benzyl radical [19].
• Enantioselectivity of some 1-[(benzofuran-2-yl) phenylmethyl] imidazoles as aromatase (P450AROM) inhibitors [20].
• The protease activity was inhibited by 5 X 10(-3) M p-chloromercuribenzoate and by phenylmethyl sulfonyl fluoride, TPCK, and soybean trypsin inhibitor, therefore the enzymatic activity probably depends on a serine residue and a sulfhydryl group [21].
• The quantitative analysis of diisopyramide and butyrophenones (BTPs) was performed in gas chromatograph equipped with packed column (glass column packed with 3% of phenylmethyl silicone-20% ph.), with previous Solid Phase Extraction (SPE) of drugs in C18 minicolumns [22].

Analytical, diagnostic and therapeutic context of methylbenzene

• The resulting mixtures were analyzed by gas-liquid chromatography (GLC) with a 65% phenylmethyl silicon open tubular fused-silica capillary column operated under optimal conditions and separated according to both their fatty acid structures and their regiospecific distribution [23].

References