High impact information on Pyridine oxide

• N-Acetylcysteine (an antioxidant) and polyvinyl pyridine-N-oxide (an agent that binds to Si-OH groups on silica surfaces) decreased AP-1 activation and phosphorylation of ERKs and p38 kinase [1].
• The results also suggest a basis for the weak carcinogenicity of NAB: facile excretion as its pyridine-N-oxide and detoxification in the esophagus by 6'-hydroxylation [2].
• By contrast, CYP3A activities were predominant in the formation of hydroxysulphone from hydroxyomeprazole as well as in the formation of pyridine-N-oxide omeprazole sulphone from omeprazole sulphone [3].
• These studies also demonstrate that the administration of ABT-299 to man results in potent, long lasting inhibition of PAF-mediated platelet activation, due in part to the pyridine-N-oxide metabolite, and support the potential therapeutic utility of this prodrug in treating PAF-mediated diseases [4].
• Pharmacokinetic studies indicated that glomerular filtration was responsible for elimination of the parent drug, and that proximal tubular secretion was the pathway of excretion of the main metabolite, pinacidil pyridine-N-oxide [5].

Biological context of Pyridine oxide

• 4. In rat, dog and man the main biotransformation product is the pyridine-N-oxide of pinacidil [6].

Anatomical context of Pyridine oxide

• The coating of quartz and kaolinite with poly-2-vinyl pyridine-N-oxide dramatically lowered their cytotoxicity towards macrophages [7].

Associations of Pyridine oxide with other chemical compounds

• Pyridine-N-oxide was found to be a quantitatively important metabolite of pyridine in all the species studied; the percentage of the dose excreted in the urine as pyridine-N-oxide ranged from 10% in rats to about 40% in mice and guinea-pigs [8].

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