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PubMed1996

Morphometric and immunohistochemical studies on atrophic changes in lympho-hematopoietic organs of rats treated with piperonyl butoxide or subjected to dietary restriction.

Changes observed in lympho-hematopoietic organs in rats given piperonyl butoxide may be attributable either to direct toxic effects or to undernutrition. Male F344 rats were therefore fed diet containing 2.5% piperonyl butoxide or subjected to a 64% restriction of food intake for 2 weeks. Marked inhibition of body weight gain, decreased white blood cell count, depletion of T/B lymphocytes in lymphoid tissues, hypoplasia of the bone marrow, and decreased proliferating cell nuclear antigen (PCNA) labeling indices in these tissues were seen in both dietary restriction and 2.5% piperonyl butoxide groups. The depletion of T lymphocytes in the thymus and spleen was stronger in the 2.5% piperonyl butoxide group, as indicated by PCNA labeling indices and image analysis of T lymphocyte areas of the spleen, however, the toxicological profile observed for the chemically treated group was essentially the same as for animals on the restricted diet. These results suggest that the lympho-hematopoietic findings in rats receiving 2.5% piperonyl butoxide are probably due to undernutrition resulting from a reduced food intake.

Animals↗

PubMed1980

The induction of hepatic cytochrome P-450 in C57 BL/10 and DBA/2 mice by isosafrole and piperonyl butoxide. A comparative study with other inducing agents.

The formation of cytochrome P-450 metabolite complexes with isosafrole and piperonyl butoxide in vivo in genetically 'responsive' C57 BL/10 mice and 'non-responsive' DBA/2 mice is described. Displacement of the isosafrole metabolite complex can be brought about by incubation with certain type I ligands. The capacity of isosafrole and piperonyl butoxide to induced cytochrome P-450 was evaluated by measurement of biphenyl 2- and 4-hydroxylase, ethoxyresofurin O-deethylase and ethylmorphine N-demethylase and by sodium dodecyl sulphate (SDS) polyacrylamide gel electrophoresis and compared with results obtained for phenobarbitone, 3-methylcholanthrene and pregnenolone-16 alpha-carbonitrile. All four monooxygenase activities were elevated by isosafrole and piperonyl butoxide, as were cytochrome P-450 levels in both strains of mice. There was a large increase in biphenyl 2-hydroxylase in microsomes from isosafrole treated mice of both strains on displacement of the metabolite complex. SDS polyacrylamide gel electrophoresis demonstrated that isosafrole and piperonyl butoxide induce protein bands of mol. wt., 54000 in both the responsive and non-responsive strains. In addition, piperonyl butoxide induces a protein band of mol. wt. 49000 in both strains of mice. The changes in metabolic activities on pretreatment with isosafrole and piperonyl butoxide do not correspond to those seen with any single inducing agent. The differences in the inducing capabilities of isosafrole and 3-methylcholanthrene in the 'non-responsive' DBA/2 strain are discussed with reference to possible mechanisms of induction by benzodioxole (methylenedioxyphenyl) compounds.

Animals↗

PubMed2002

Plasma achiral and chiral pharmacokinetic behaviour of intravenous oxfendazole co-administered with piperonyl butoxide in sheep.

Co-administration of piperonyl butoxide (PB) potentiates fenbendazole (FBZ) in small ruminants. The resultant increase in bioavailability of FBZ and its metabolite oxfendazole (OFZ) has important implications for the efficacy of these drugs against benzimidazole (BZD)-resistant strains of Teladorsagia circumcincta. This study evaluated the racemic (achiral) and enantiomeric (chiral) plasma disposition kinetics of OFZ and its metabolites after the co-administration of PB and OFZ in sheep. Six 6-8-month-old, parasite-free, female Dorset sheep (30-40 kg) were used in a two-phase crossover experiment. In phase I, three sheep received 30 mg/kg PB orally, followed by a single intravenous (i.v.) injection of OFZ at 5 mg/kg. The other three animals were treated similarly except that 5 mL of water replaced PB. In phase 2, treatments for the two groups were reversed and were given 14 days after the initiation of phase I. Three analytes OFZ, FBZ and fenbendazole sulphone (FBZSO(2)) were recovered in plasma up to 48 h post-treatment in both experimental groups. Achiral and chiral pharmacokinetic (PK) profiles for OFZ, after the co-administration of PB, were characterized by a significantly greater area under the concentration--time curve (AUC) and a longer mean residence time (MRT). Chiral OFZ distribution ratios were comparable in both treatment groups. Piperonyl butoxide treatment markedly influenced the plasma PK profiles for FBZ and FBZSO(2) following OFZ administration. Production of FBZ was enhanced as reflected by increased (> 60%) AUC, delayed T(max) and a significantly delayed (> 45%) elimination (t(1/2)(el)). Although AUC values for FBZSO(2) were not significantly different between groups, this metabolite was depleted more slowly from plasma (t(1/2)(el) > 60% and MRT > 42%) following PB treatment. This study demonstrated that PB co-administration is associated with an inhibition of OFZ biotransformation, as evidenced by the significantly higher plasma concentrations of OFZ and FBZ, and this could have important implications in terms of anti-parasite therapy against BZD-resistant parasite strains.

Administration, Oral↗

PubMed1987

Comparison of pediculicidal and ovicidal effects of two pyrethrin-piperonyl-butoxide agents.

A pyrethrin-piperonyl-butoxide shampoo was compared with a similarly formulated lotion for their pediculicidal and ovicidal effects against head lice. Forty children with active Pediculus humanus capitis infestation were randomly assigned to one of two groups for a single treatment with either the shampoo or the lotion. An average of ten nits were taken from each patient both before and after treatment. These eggs were incubated for 14 days, the resulting lice counted, and their conditions noted. Lice recovered from the rinse water after treatment were also counted and observed. Although both products proved to be effective in killing lice, the shampoo had greater ovicidal efficacy, 50% versus 25% for the lotion, after adjustment for natural mortality of the ova.

Administration, Topical↗

PubMed1992

Effects of piperonyl butoxide on F1 generation mice.

Piperonyl butoxide (PB), used in Japan as a pesticide synergist and food additive, was administered to mice from 5 weeks of age in the F0 generation to 9 weeks of age in the F1 generation, in the diet at levels of 0 (control), 0.15, 0.30 and 0.60%, and some reproductive, developmental and behavioral parameters were measured. Some parameters of open field activity were reduced in the treatment groups; in particular, ambulation and rearing were significantly reduced in F0 generation male mice and in 3-week-old F1 generation male mice. The weight of the pups was significantly reduced and litter weight tended to be reduced in the treatment groups. Body weight of dosed pups was reduced in the lactation period. Of the developmental parameters, olfactory orientation was significantly reduced as compared to controls. The dose levels of PB in this study, therefore, had an effect on some reproductive, developmental and behavioral parameters in mice.

Animals↗

PubMed2006

Metabolism and excretion of piperonyl butoxide in the rat.

[14C]-piperonyl butoxide (PBO) was administered to male and female rats by gavage at a dose rate of 50 or 500 mg kg-1 body weight. In all cases, the radioactivity was rapidly excreted with 87-99% being found in the 0-48-h excreta and the majority of the dose (64.1-85.0%) being eliminated in faeces. The metabolism of PBO was complex with over 25 peaks of radioactivity being seen by radio-high-performance liquid chromatography (HPLC). Using HPLC/tandem mass spectrometry (MS/MS) and nuclear magnetic resonance (NMR), 12 urine metabolites were assigned structures together with four plus PBO in faeces. Metabolism occurred at two sites: the methylenedioxy ring, which opened to form a catechol that could then undergo methylation, and the 2-(2-butoxyethoxy)ethoxymethyl side-chain, which underwent sequential oxidation to a series of alcohols and acids. The identified metabolites accounted for approximately 60% of the administered dose.

Administration, Oral↗

PubMed1992

Evaluation of three candidate cypermethrin-piperonyl butoxide formulations compared with Scourge against adult Culex quinquefasciatus.

Cypermethrin-piperonyl butoxide formulations (1:1, 1:5, 1:10) were evaluated in a laboratory wind tunnel against colony reared, susceptible adult Culex quinquefasciatus mosquitoes. Scourge (4% resmethrin:12% piperonyl butoxide) was used as the standard for comparison. Based on the LC90 data, the 3 cypermethrin-piperonyl butoxide formulations were 2.6-3.7x more toxic than Scourge 24-h posttreatment.

Animals↗

PubMed1998

Effect of piperonyl butoxide or allopurinol on cyanide-induced lipid peroxidation in mouse brain.

The effect of piperonyl butoxide or allopurinol on cyanide-induced lipid peroxidation was investigated using homogenates from whole brain of mice. The brain homogenate exposed to a low concentration of potassium cyanide (10, 50, or 100 microM) was significantly increased in their concentration of malondialdehyde (MDA) + 4-hydroxyalkenals (4-MDA) as compared to control samples, in a concentration-dependent manner. The increased lipid peroxidation induced by cyanide was inhibited by piperonyl butoxide (1 mM), an inhibitor of mixed function oxidase, but not by allopurinol (0.1 mM), an inhibitor of xanthine oxidase. Furthermore, when a brain homogenate heated at 86 degrees C for 1 min was incubated with or without cyanide at 37 degrees C for 20 min, MDA + 4-MDA levels in the homogenate were not changed between cyanide treatment and untreated. An intraperitoneal injection of piperonyl butoxide (1 g/kg) significantly inhibited cyanide-induced seizures in mice. These results suggest that cyanide-induced seizures may be partly involved in the lipid peroxidation produced by the heat unstable and piperonyl butoxide dependent factors in brain.

Allopurinol↗

PubMed1994

Chronic toxicity studies of piperonyl butoxide in F344 rats: induction of hepatocellular carcinoma.

Male and female F344 rats (30-33 rats/group) were administered piperonyl butoxide (alpha-[2-(2-butoxyethoxy)ethoxy]-4,5-methylenedioxy-2-propylto luene) in the diet at levels of 0 (control), 0.6, 1.2, and 2.4% for nearly 2 years. Beginning at about 40 weeks, 10 rats in the 1.2% treated male group died due to cecal hemorrhages. Piperonyl butoxide induced hepatocellular carcinoma in both sexes in a dose-dependent manner. Hepatocellular carcinoma was found even in the 1.2% treated male group (incidence, 26.7%), and incidences in the 2.4% groups of males and females were 80.0 and 57.7% respectively of all those surviving. Piperonyl butoxide also caused essential thrombocythemia with a dose-response relationship. Hemorrhages in stomach and cecum, anemia, degenerative lesions of alveoli, and nephrotoxicity were also observed related to exposure. These results indicate that piperonyl butoxide is a hepatocarcinogen to the rat.

Animals↗

PubMed1983

Effects of piperonyl butoxide on cephalosporin nephrotoxicity in the rabbit. An effect on cephaloridine transport.

To evaluate the hypothesis that cytochrome P-450 mixed-function oxidase (MFO) activity may have a causal role in the production of cephalosporin nephrotoxicity, the effects of the MFO inhibitors cobaltous chloride and piperonyl butoxide on the nephrotoxicity of cephaloridine in the rabbit were examined. Although cobaltous chloride had no effect on cephaloridine nephrotoxicity, piperonyl butoxide had a significant protective effect. However, in correlated studies of the effects on the renal cortical uptake and disappearance of cephaloridine, it was found that piperonyl butoxide significantly reduces (by 50%) the cortical concentrations of the cephalosporin, both decreasing its uptake by and increasing its disappearance from tubular cells. Finally, we evaluated the effect of piperonyl butoxide on the nephrotoxicity of cephaloglycin, a more toxic cephalosporin that lacks the thiophene side-ring proposed as the target of MFO activation in earlier studies with cephaloridine. No protection against cephaloglycin was found. 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.

Acute Kidney Injury↗

PubMed1994

Piperonyl butoxide induces hepatocellular carcinoma in male CD-1 mice.

Male CD-1 mice in groups of 52, 53 or 100 were administered piperonyl butoxide (alpha-[2-(2-butoxyethoxy)ethoxy-4,5-methylenedioxy-2-propyltol uene) in the diet at levels of 0 (control), 0.6 and 1.2% for 12 months. Hepatocellular carcinoma was induced in treated groups in a dose-dependent manner but not in the control group. The incidences of hepatocellular carcinoma were 11.3 and 52.0% in mice given 0.6 and 1.2% piperonyl butoxide, indicating that piperonyl butoxide can cause hepatocellular carcinoma in mice as it is known to do in rats.

Animals↗

PubMed1985

Lack of evidence of carcinogenicity of technical-grade piperonyl butoxide in F344 rats: selective induction of ileocaecal ulcers.

The carcinogenicity of technical-grade piperonyl butoxide was studied in F344/DuCrj rats fed a dietary level of 0.5 or 1% for 2 yr. Various tumours were detected in all groups, including the untreated control group, but no significant dose-related increase in the incidence of any tumour was found. Thus, it is concluded that under these experimental conditions piperonyl butoxide was not carcinogenic in F344 rats. Unexpectedly, however, ileocaecal ulcers were found in animals of both sexes in both experimental groups and the incidence was dose related. Further studies are required to establish the mechanism of induction of ileocaecal ulcers by piperonyl butoxide.

Administration, Oral↗

PubMed1995

Piperonyl butoxide mutagenicity in human RSa cells.

Piperonyl butoxide (PB) is used as a pesticide synergist and food additive. Its chemically induced mutagenicity was found in cultured human RSa cells by determination of ouabain-resistant (Ouar) phenotypic mutation, with the highest frequency at the concentration of 0.2 microgram/ml. Moreover, K-ras codon 12 mutations in genomic DNA, analyzed by polymerase chain reaction (PCR) and differential dot-blot hybridization using digoxigenin-labeled probes, were detected in RSa cells 6 days after exposure to PB (0.03-0.40 microgram/ml).

Base Sequence↗

PubMed1997

Chronic toxicity studies of piperonyl butoxide in CD-1 mice: induction of hepatocellular carcinoma.

Male and female CD-1 mice (51-104 mice/group) were administered piperonyl butoxide (alpha-[2-(2-butoxyethoxy)ethoxy-4,5-methylenedioxy-2-propyltol uene) in the diet at levels of 0 (control), 0.6 and 1.2% for 52 weeks (1 year). Hepatocellular carcinomas were induced in treated groups in a dose-dependent manner. The incidences of hepatocellular carcinoma were 11.3 and 52.0% in male mice given 0.6 and 1.2% piperonyl butoxide, and 41.2% in female mice given 1.2%. Piperonyl butoxide is thus a hepatocarcinogen to mice as it is known to be to rats.

Animals↗

PubMed1991

Piperonyl butoxide as a tool in aquatic toxicological research with organophosphate insecticides.

Experiments were conducted to determine the effects of piperonyl butoxide, a synthetic methylenedioxyphenyl inhibitor of cytochrome(s) P450, on the toxicity of organophosphate insecticides to three cladoceran test species: Ceriodaphnia dubia. Daphnia magna, and Daphnia pulex. Coadministration of piperonyl butoxide effectively reduced the acute toxicity of four metabolically activated organophosphates (parathion, methyl parathion, diazinon, and malathion) and did not affect the toxicity of three organophosphates not requiring metabolic activation (dichlorvos, chlorfenvinphos, and mevinphos). These results indicate that piperonyl butoxide may be an effective tool in toxicological research focused upon identifying specific compounds responsible for toxicity in complex aqueous mixtures.

Animals↗

PubMed1991

Differences in the effects of piperine and piperonyl butoxide on hepatic drug-metabolizing enzyme system in rats.

An i.p. administration of rats with piperine (100 mg/kg) and piperonyl butoxide (400 mg/kg) produced a significant decrease in hepatic cytochrome P-450, and activities of benzphetamine N-demethylase, aminopyrine N-demethylase and aniline hydroxylase 1 hr after the treatment. Twenty-four hr later, these parameters along with cytochrome b5 and NADPH-cytochrome c reductase remained depressed only in piperine-treated rats. In contrast, piperonyl butoxide caused a significant induction of these parameters with the exception of cytochrome b5 and aminopyrine N-demethylase, which were up by 36 and 33% over their respective controls but not significantly. These results point up that effect of piperine on hepatic mixed-function oxidases is monophasic while that of piperonyl butoxide is biphasic.

Alkaloids↗

PubMed1979

Carcinogenesis bioassay of technical-grade piperonyl butoxide in F344 rats.

The insecticide synergist piperonyl butoxide--alpha-[2-(2-butoxyethoxy)ethoxy]-4,5-methylenedioxy-2-propyltoluene--was tested for carcinogenicity in inbred F344 rats in a 2-year study employing doses of 10,000 and 5,000 ppm of the compound administered continuously in the feed. Although a statistically significant dose-related increase in the incidence of lymphoreticular neoplasia was associated with administration of the compound to females, the incidence of that class of neoplasm was higher in control males than in treated males. The finding of statistical significance in one sex is not considered by itself to constitute sufficient evidence of a biologic effect to justify an indictment of carcinogenic action. However, inasmuch as the chief use of this substance is to alter the in vivo metabolism of other chemicals, its possible role as a cocarcinogen should be carefully considered in any risk-benefit evaluation aimed at setting policies regarding its uses.

Animals↗

PubMed2001

Comparative evaluation of new synergists containing a butynyl-type synergophore group and piperonyl butoxide derivatives.

Cross-substituted derivatives of piperonyl butoxide (PBO) and MB-599 (proposed common name: verbutin) were synthesized and investigated as carbofuran and permethrin synergists against housefly, Musca domestica L. The majority of PBO and MB-599 derivatives were significantly more potent synergists for carbofuran than for permethrin. PBO, the most important representative of this series was not the most potent synergist for carbofuran or for permethrin. Cleavage of the methylenedioxy ring of methylenedioxyphenyl (MDP) polyether compounds resulted in complete loss of synergistic activity with both insecticides, but it could be restored or even improved by incorporating an alkynyl ether moiety into the molecule. The improved synergistic activity was found to be closely associated with the 2-butynyloxymethyl side-chain, suggesting that this can be regarded as a characteristic synergophore group. MB-599, one of the most promising compounds bearing this group showed considerably higher activity with carbofuran (synergist ratio, SR = 37.8) than with PBO (SR = 6.4). There was no significant difference between synergistic activities of MB-599 (SR = 4.6) and PBO (SR = 4) for permethrin.

Alkynes↗