3420-97-1Relevant articles and documents
Ipso-Nitrosation of arylboronic acids with chlorotrimethylsilane and sodium nitrite
Prakash, G.K. Surya,Gurung, Laxman,Schmid, Philipp Christoph,Wang, Fang,Thomas, Tisa Elizabeth,Panja, Chiradeep,Mathew, Thomas,Olah, George A.
, p. 1975 - 1978 (2014/04/03)
Nitroso compounds are versatile reagents in synthetic organic chemistry. Herein, we disclose a feasible protocol for the ipso-nitrosation of aryl boronic acids using chlorotrimethylsilane-sodium nitrite unison as nitrosation reagent system.
New nitrite ionic liquid (IL-ONO) and nanoparticles of organosilane-based nitrite ionic liquid immobilized on silica as nitrosonium sources for electrophilic aromatic nitrosation
Valizadeh, Hassan,Amiri, Mohammad,Shomali, Ashkan
experimental part, p. 1103 - 1108 (2012/03/10)
An improved method for the synthesis of nitrosoarenes has been developed using a new nitrite ionic liquid (IL-ONO) and immobilized nitrite ionic liquid. These ionic liquids play as nitrosonium sources for electrophilic aromatic nitrosation of active aromatics at 0-5 °C. Their action was accomplished in water and the satisfactory results were obtained under the mild conditions in short reaction time.
Mechanism of metabolic activation of the analgetic bucetin to bacterial mutagens by hamster liver microsomes
Nohmi,Ishidate Jr.,Hiratsuka,Watabe
, p. 2877 - 2885 (2007/10/02)
Bucetin (N-(β-hydroxybutyryl)-p-phenetidine) was found to be mutagenic to Salmonella typhimurium TA100 in the presence of liver 9000 g supernatant fractions (S9) prepared from polychlorinated biphenyl (PCB)-treated hamsters and a reduced nicotinamide adenine dinucleotidephosphate (NADPH)-generating system. However, the analgetic was not mutagenic in the presence of NADPH-fortified S9 from PCB-treated rat liver. The mutagenic potency of bucetin was about a quarter of that of the structurally related analgetic, phenacetin. PCB-treated hamster liver microsomes fortified with NADPH activated bucetin to two direct-acting mutagens, N-hydroxy-phenetidine and p-nitrosophenetole, through deacylation followed by N-hydroxylation. The nitroso compound arose from N-hydroxyphenetidine via autoxidation. N-(b-Hydroxybutyryl)-p-amino-phenol, a major metabolite of bucetin under the conditions used, was not mutagenic to TA100 either with or without NADPH-fortified S9 from PCB-treated or untreated rats or hamsters. N-Hydroxybucetin, which was about 70 times less mutagenic than N-hydroxyphenacetin in the presence of PCB-treated hamster S9, was not detected as a metabolite of bucetin from the NADPH-fortified reaction mixtures. Although no species difference was observed in p-phenetidine N-hydroxylation, the rate of bucetin deacylation was over 90 times higher in hamsters than in rats. The rate of microsomal deacylation of bucetin was much lower than that of phenacetin or N-butyryl-p-phenetidine. These results suggest that the species difference in bucetin mutagenicity is due to the difference in deacylating activity between rat and hamster liver microsomes, and also that the β-hydroxyl group in the butyryl side chain makes bucetin poorly hydrolyzable in microsomes, resulting in lower mutagenic activity as compared with phenacetin.