Disease relevance of PIPERONYL BUTOXIDE

• 1-(4-Chlorophenyl)-4-cyclohexyl-bicycloorthocarboxylate is particularly sensitive to oxidative detoxification based on its 10-fold synergism of toxicity by piperonyl butoxide and marked potency loss in a coupled [35S]TBPS receptor/microsomal oxidase assay [1].
• Lindane 1%, permethrin 1%, and pyrethrins with piperonyl butoxide are all effective treatments for pediculosis [2].
• Cuprizone and piperonyl butoxide, proposed inhibitors of T-cell function, attenuate experimental allergic encephalomyelitis in SJL mice [3].
• In an effort to combat West Nile Virus, planes dispersed insecticide over Sacramento, CA, treating nearly 50,000 hectares with pyrethrins and the synergist piperonyl butoxide (PBO) [4].
• Piperonyl butoxide induces hepatocellular carcinoma in male CD-1 mice [5].

Psychiatry related information on PIPERONYL BUTOXIDE

• Piperonyl butoxide, a microsomal monooxygenase inhibitor, administered intraperitoneally to mice exerts peak anti-maximal electroshock activity and peak neurotoxicity at 5 and 7h, respectively [6].
• The animals performed three trials in multiple water T-maze at 10 weeks of age, and the number of errors was significantly decreased in treatment groups on the 3rd trial, while there was no biologically significant effect of piperonyl butoxide on maze learning [7].
• From these results, piperonyl butoxide showed adverse effects on the motor activity of the exploratory behaviour in male mice [7].
• The effects of these compounds on the feeding behavior and performance (with and without piperonyl butoxide pretreatment) of Spodoptera littoralis larvae and Leptinotarsa decemlineata adults indicate that some strongly deterred these insects, L. decemlineata being less sensitive than S. littoralis [8].

High impact information on PIPERONYL BUTOXIDE

• Prior treatment of the microsomes with piperonyl butoxide or another mixed-function oxidase inhibitor markedly decreases the activation [9].
• Piperonyl butoxide also protects against brain acetylcholinesterase inhibition and cholinergic symptoms in chicks resulting from (-)-profenofos administration, thus establishing the importance of the oxidative bioactivation of S-alkyl phosphorothiolate pesticides in vivo [9].
• (i) The effect of a specific P450 inhibitor, piperonyl butoxide, on larval survival through eclosion on each cactus substrate was investigated [10].
• Blockers of the cytochrome P-450 epoxygenase, such as SKF 525A and piperonyl butoxide, compounds that have different molecular structures, also suppressed secretagogue-induced ACTH release [11].
• At 60 min, the amount of isaxonine metabolite covalently bound per mg of protein was similar in plasma membranes (0.42 nmole metabolite.mg protein-1) and in microsomes (0.38); both values were decreased by about 70% in rats pretreated with piperonyl butoxide, an inhibitor of cytochrome P-450 [12].

Chemical compound and disease context of PIPERONYL BUTOXIDE

• The covalent binding and toxicity of 4-ipomeanol to the renal tubules could be prevented by pretreatment of the animals with piperonyl butoxide [13].
• It is concluded that these inhibitors of MFO activity do not reduce cephalosporin nephrotoxicity in general, and that the reduction of cephaloridine toxicity by piperonyl butoxide can be explained by an effect on the intracellular concentrations of that particular cephalosporin [14].
• A ternary mixture of acetylcholinesterase inhibiting organophosphates (malathion and parathion) and the P450 inhibitor piperonyl butoxide was used to model toxicity [15].
• Pyrene toxicity was explained by the body residues of parent pyrene and PBO, where the metabolites' contribution was negligible [16].
• Since the APAP-induced inhibition of mitochondrial respiration, in vivo, correlated with age-related and piperonyl butoxide-dependent differences in toxicity, the data suggest that the in vivo effects result, at least in part, from a mixed-function oxidase generated metabolite [17].

Biological context of PIPERONYL BUTOXIDE

• Naphthalene-induced decreases in cell viability were blocked by preincubation of Clara cells with the cytochrome P450 monooxygenase inhibitor piperonyl butoxide [18].
• In a second series of experiments, in vitro metabolic activation was demonstrated with human liver microsomes; as in mice, covalent binding required NADPH and was markedly inhibited by piperonyl butoxide [19].
• Piperonyl butoxide pretreatment markedly increased the half-life of PCA in brain, but it failed to modify consistently the effects of PCA [20].
• The effect of piperonyl butoxide, a P450 inhibitor, on the fungal conversion of 1-dodecanol was also investigated, indicating that hydroxylation reactions of 1-dodecanol were inhibited by piperonyl butoxide in a concentration-dependent manner [21].
• Piperonyl butoxide was administered to pregnant rats by gavage at a level of 0 (control), 630, 1065, and 1800 mg/kg bw on days 11-12 of gestation [22].

Anatomical context of PIPERONYL BUTOXIDE

• However, treatment of hepatocytes in vitro with metyrapone or piperonyl butoxide, two general inhibitors of P-450 enzymes, inhibited the binding of 2,4-DAT to DNA by approximately 80-85% [23].
• Uroporphyrin accumulation produced by halogenated biphenyls in chick-embryo hepatocytes. Reversal of the accumulation by piperonyl butoxide [24].
• In an in vitro study, the effect of cytochrome P-450 inhibitors, cimetidine or piperonyl butoxide, on cisplatin-induced cytotoxicity and catalytic iron release from LLC-PK1 cells was examined [25].
• Cuprizone, a copper chelator, and piperonyl butoxide (PBO), a pesticide synergist, are implicated to inhibit T-cell activation and function [3].
• However, the administration of THC to estrogen-replaced ovariectomized rats that had been pretreated with two separately administered inhibitors of cytochrome P450, piperonyl butoxide or metyrapone, significantly increased DOPAC content in the medial basal hypothalamus, with no changes in the other parameters [26].

Associations of PIPERONYL BUTOXIDE with other chemical compounds

• The chloroperoxidase-catalyzed demethylations were inhibited by inhibitors of cytochrome P-450 such as azide or n-propyl gallate, but not by metyrapone, SKF-525A, or piperonyl butoxide [27].
• Aminopyrine N-demethylase activity in mouse brain microsomes was dependent on the presence of oxygen and NADPH and could be inhibited by piperonyl butoxide, N-octyl imidazole and carbon monoxide [28].
• Concomitant treatment of the cells with inhibitors of cytochrome P450 monooxygenases (SKF-525A, piperonyl butoxide or carbon monoxide) did not alter the inhibition of GJIC by the cyclodienes, suggesting that cytochrome P450 metabolism was not involved in the inhibitory mechanism [29].
• TSH, NE, and arachidonic acid stimulation of I- efflux in FRTL-5 cells is associated with increased iodination of thyroglobulin, which is blocked by 10 microM 5,8,11,14-eicosatetraynoic acid and 50 microM piperonyl butoxide [30].
• Analysis of mice injected with one or both drugs showed that piperonyl butoxide augmented the effects of PDMP on ceramide, glucosylceramide, and dihexosylceramide levels, as well as on the activity of glucosylceramide synthase [31].

Gene context of PIPERONYL BUTOXIDE

• The NADPH-dependency and the inhibitory effect of carbon monoxide and piperonyl butoxide on taxol metabolism indicated the involvement of cytochrome P450 (CYP) monooxygenases [32].
• Partial and almost complete reversion to susceptibility as larvae was achieved with S, S, S-tributylphosphorotrithioate and piperonyl butoxide (PBO), respectively, suggesting the presence of carboxylesterase and P450 monooxygenase mediated resistance [33].
• It is suggested that piperonyl butoxide be used as an adjuvant for the many useful drugs that are inactivated by the P450 system [31].
• This enzyme reaction was inhibited by cytochrome P450 inhibitors such as piperonyl butoxide, SKF-525A, paclobutorazole, metyrapone, cytochrome c, and carbon monoxide [34].
• Piperonyl butoxide was tested for mutation with and without metabolic activation in the CHO/HGPRT assay [35].

Analytical, diagnostic and therapeutic context of PIPERONYL BUTOXIDE

• Carcinogenesis bioassay of technical-grade piperonyl butoxide in F344 rats [36].
• A new method for determination of pyrethroids, pyrethrins, and piperonyl butoxide (PBO) by high-resolution gas chromatography/high-resolution mass spectrometry (HRGC/HRMS) was developed for aquatic sediments [37].
• Determination of traces of pyrethrins and piperonyl butoxide in biological material by high-performance liquid chromatography [38].
• After treatment with the cytochrome P450 inhibitor piperonyl butoxide, the above relations ceased to apply, but this treatment did not influence the kinetics of paraoxon and parathion uptake [39].
• An HPLC method for the simultaneous determination of safrole (S), dihydrosafrole (DHS), and chloromethyldihydrosafrole (CM-DHS) in piperonyl butoxide, with fluorimetric detection and elution gradient, is described [40].

References