Disease relevance of NSC 126828

• Correction of ischaemic brain acidosis with SQ29,548/1-benzylimidazole [1].
• We studied the effect of a selective thromboxane A2 (TxA2) synthetase inhibitor, 1-benzylimidazole (BIm), on the immune complex glomerulonephritis produced by bovine serum albumin (BSA) in New Zealand white rabbits [2].

High impact information on NSC 126828

• On the other hand, these in vitro studies showed that the increase in microsomal epoxide hydrolase activity by 1-benzylimidazole may partially be due to activation of the enzyme [3].
• 1-Benzylimidazole induced both cytosolic epoxide hydrolase and peroxisomal beta-oxidation activity about 2-fold, whereas microsomal epoxide hydrolase activity was increased about 4-fold [3].
• This activation of MBT is almost completely blocked by the cytochrome P450 inhibitor N-benzylimidazole but not by several other cytochrome P450 inactivators [4].
• On the other hand, there was essentially no difference in the induced levels of CYP1A1/2 apoprotein and mRNA between twins of SDR and EHBR/Eis livers treated with 3-methylcholanthrene or 1-benzylimidazole [5].
• 3. The bleeding time of the rat endometrium was unchanged from control values following treatment with prostacyclin (0.5 microgram kg-1 min-1, i.v.) or 1-benzylimidazole (50 mg kg-1, i.v.) whereas the bleeding times were increased in the rat mesentric artery [6].

Biological context of NSC 126828

• In isolated ventricular strips of rabbits, 6.3 times 10(-5) M 1-benzylimidazole (BI) increased contractile force by 100%, and in the intact cat, 0.5 mg/kg of BI increased cardiac output by 30 to 40% [7].
• Pretreatment with 1-benzylimidazole restored renal function, eicosanoid release, and renal blood flow to sham levels [8].
• Pre-incubation of 2AA in the presence of N-benzylimidazole significantly increased the activation of 2AA by S9 from BNF- and PB-treated rats, which suggests that CYPs play minor role in 2AA metabolic activation by rat liver S9 fractions [9].

Anatomical context of NSC 126828

• The formation of DETC-MeSO was blocked completely by solubilization of the microsomes with the detergent Emulgen 911, or by the presence of the cytochrome P450 inhibitor 1-benzylimidazole [10].
• MeDDC metabolism in human liver microsomes was studied by using either heat inactivation to inhibit FMO, or N-benzylimidazole (NBI) or antibodies to the CYP450 NADPH reductase to inhibit CYP450 [11].
• The present work investigated the ability of the N-imidazole derivative, 1-benzylimidazole (BIM), to induce CYP1A in rainbow trout hepatocytes [12].
• We administered a TXA2 receptor antagonist, SQ29,548, and a thromboxane A synthase inhibitor, 1-benzylimidazole (1-BI), to rats subjected to 30 min of reversible forebrain ischaemia [1].

Associations of NSC 126828 with other chemical compounds

• This reaction was dependent on NADPH and molecular oxygen and was inhibited by CO and 1-benzylimidazole [13].
• When glutathione S-transferase activity was measured with cis-stilbene oxide as substrate only the more than five-fold increase after treatment with 1-benzylimidazole was significantly different from control values [14].
• 1,3-Butadiene metabolism was NADPH-dependent and inhibited by 1-benzylimidazole [15].
• Inclusion of both phospholipid and a tight-binding nitrogenous ligand, 1-benzylimidazole, in the reaction medium produces a burst-phase of DTNB modification, but the stoichiometry remains one thiol modified per polypeptide chain [16].
• This study was undertaken to determine if rCBF could be elevated by postischemic treatment with a TXA2 receptor antagonist, SQ29,548, given alone or in combination with 1-benzylimidazole (1-BI), a thromboxane synthase inhibitor [17].

Gene context of NSC 126828

• We examined the effect of 1-benzylimidazole on the induction of cytochrome P-450 1A1/2 (P-450 1A1/2) and cytochrome P-450 2B1/2 (P-450 2B1/2) in normal, castrated, ovariectomized and hypophysectomized male rats, and in castrated rats treated with testosterone [18].
• Scavengers of hydrogen peroxide and hydroxyl radicals, including catalase and benzoate and inhibitors of microsomal cytochrome P-450-dependent monooxygenases such as 1-benzylimidazole, metyrapone and alpha-naphthoflavone, had no inhibitory effects on bleomycin-mediated DNA chain breakage [19].
• However, 1-benzylimidazole failed to bind with high affinity to the cytosolic Ah receptor [20].
• N-benzylimidazole, a nonspecific CYP inhibitor, and various CYP isoform selective inhibitors did not affect BZD N-oxidation [21].
• Inclusion of the cytochrome P450 inhibitor 1-benzylimidazole inhibited 1,3-butadiene metabolism, but inclusion of KCN, catalase, or superoxide dismutase had no effect [22].

Analytical, diagnostic and therapeutic context of NSC 126828

• Activity of dihydrodiol dehydrogenase was increased after treatment of rats with 1-benzylimidazole (1.5-fold), whereas application of tiadenol led to a decrease of enzyme activity [14].
• The determination of the concentration in microsomal epoxide hydrolase by immunoassay revealed no change in the protein amount within the membrane; only the specific activity was enhanced by bezafibrate and 1-benzylimidazole, suggesting an activation process [23].

References