Disease relevance of Phenylimidazole

• Cotreatment with the cytochrome P450 inhibitor 1-phenylimidazole prevented both cytolethality and GSH depletion, indicating that metabolism is necessary for chloroform-induced toxicity [1].
• Interplanar torsion in the S1<--S0 electronic spectrum of jet cooled 1-phenylimidazole [2].

High impact information on Phenylimidazole

• Treatment of isolated rat hepatocytes with diethylmaleate decreased covalent binding of EDB to DNA, but treatment with 1-phenylimidazole did not, consistent with the view that conjugative metabolism is of greater importance than oxidation with regard to DNA binding [3].
• 1-Phenylimidazole did not bind to wild-type eNOS heme, but bound to all Asp-369 and Arg-372 mutants (Kd ranged from 10 to 65 microM) except R372K [4].
• Active-site structures of the mutants were probed with the inhibitors 12-(imidazolyl)dodecanoic acid and 1-phenylimidazole [5].
• The P450 ligand 1-phenylimidazole and substrate ethanol were potent inhibitors of ACN epoxidation after all treatments [6].
• The isozyme-selective P-450 inhibitor alpha-naphthoflavone (ANF) potently inhibited the high-affinity component of caffeine N-demethylations, while 1-phenylimidazole (PI) was a more potent inhibitor of the low-affinity component [7].

Biological context of Phenylimidazole

• Furan-mediated depletion of ATP occurred prior to cell death and was prevented by including 1-phenylimidazole, a cytochrome P450 inhibitor, in the suspensions [8].
• The major objectives were to investigate substrate specificities of the series in human microsomes and interspecies variation for the prototype molecule, 1-phenylimidazole [9].
• CG base pair recognition by substituted phenylimidazole nucleosides [10].
• N-Phenylimidazole, a specific cytochrome P-450 inhibitor, also lowers the efficiency of bacteroid oxidative phosphorylation [11].
• The P450 inhibitors phenylimidazole, benzylimidazole prevented the metabolic activation of phenelzine but not lipid peroxidation [12].

Anatomical context of Phenylimidazole

• The structural identity of the metabolite formed by incubation of 1-phenylimidazole with human liver microsomes was proven to be the N(+)-glucuronide by exhibiting the same HPLC retention time and electrospray ionization mass spectrum as the reference sample [13].
• Feeding of these compounds in combination with the inhibition of cytochrome P-450 by 1-phenylimidazole (PhI) allowed sufficient quantities of the mutagen to reach the gonads and to produce significant genetic damage [14].

Associations of Phenylimidazole with other chemical compounds

• The utility of the visible assay is further demonstrated by the simple determinations of the coupling ratio for 7-ethoxyresorufin oxidation in scup liver microsomes and the K1 for 7,8-benzoflavone and phenylimidazole inhibition of the enzymatic reaction [15].
• The enzyme-inhibiting activities of PhI and Ipr were determined in vitro using microsomes obtained from Drosophila larvae and adults [16].
• Metyrapone and phenylimidazole, chemical inhibitors of cytochrome P-450, also relax the ductus [17].
• Both carbon dioxide production and cell binding were significantly inhibited by a general inhibitor of cytochrome P-450 activity (carbon monoxide) and by specific P-450 2E1 inhibitors (chlorzoxazone, isoniazid, 4-methylpyrazole and 1-phenylimidazole) [18].

Gene context of Phenylimidazole

• UGT1A3 also catalyzed the glucuronidation of the previously investigated 1-phenylimidazole but none of the newly investigated compounds [19].
• 1-Phenylimidazole (PhI) is used as an inhibitor of the cytochrome P-450 (P-450) mediated monooxygenase activities [16].

References