Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Pesticide Synergists”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2002

Synergistic effects of pesticides and metals on the fibrillation of alpha-synuclein: implications for Parkinson's disease.

Aggregation of alpha-synuclein has been implicated in the formation of proteinaceous inclusions in the brain (Lewy bodies, Lewy neurites) that are characteristic of neurodegenerative diseases, such as Parkinson's disease (PD) and dementia with Lewy bodies (DLBs). The etiology of PD is unknown, but recent work has shown that except in rare cases, there appears to be no direct genetic basis. However, several studies have implicated environmental factors, especially pesticides and metals. Here we show that certain pesticides and metals induce a conformational change in alpha-synuclein and directly accelerate the rate of formation of alpha-synuclein fibrils in vitro. In addition, the simultaneous presence of metal and pesticide led to synergistic effects on the rate of fibrillation. We propose a model in which environmentalfactors in conjunction with genetic susceptibility may form the underlying molecular basis for idiopathic PD.

Aluminum Chloride↗
PubMed2001

Cuprizone and piperonyl butoxide, proposed inhibitors of T-cell function, attenuate experimental allergic encephalomyelitis in SJL mice.

Multiple sclerosis (MS) and its animal model, experimental allergic encephalomyelitis (EAE), are autoimmune demyelinating diseases with autoreactive T-cells acting as important mediators of pathogenesis. Cuprizone, a copper chelator, and piperonyl butoxide (PBO), a pesticide synergist, are implicated to inhibit T-cell activation and function. The purpose of this study was to assess whether either of these agents would suppress PLP-peptide-induced EAE in the SJL mouse. Indeed, treatment with cuprizone beginning 1 week prior to disease induction, and PBO administration from days 1 to 9 of EAE, significantly attenuated EAE clinical severity. Furthermore, both agents decreased blood CD4+/CD8+ ratios, and reduced signs of chronic graft vs. host disease (GVHD) indicating attenuation of an immune T-cell response. These results suggest that cuprizone and PBO suppress EAE and use of these agents will provide insights into the mechanisms of T-cell mediated diseases.

Animals↗
PubMedDate not supplied

Liquid chromatographic determination of N-methyl carbamate pesticide residues at low parts-per-billion levels in eggs.

A reversed-phase liquid chromatographic (LC) method is presented for the analysis of N-methyl carbamate pesticide residues and piperonyl butoxide in eggs at levels as low as 2 microg/kg (ppb). The study was undertaken to provide data for dietary exposure estimates used in risk analysis. The method uses an acetonitrile extraction followed by liquid-liquid partitioning and normal-phase aminopropyl solid-phase extraction column cleanup. Determination of residues is by reversed-phase LC with an inline postcolumn reaction followed by fluorescence detection. The average recoveries of 21 fortified (most at 2.0 and 20.0 ppb) N-methyl carbamate pesticide residues and the carbamate metabolite 1-naphthol from eggs ranged from 70 to 107%. Recoveries of the pesticide synergist piperonyl butoxide ranged from 63 to 106%. Single-comb White Leghorn hens were treated with the carbamate carbaryl, and the eggs subsequently produced were analyzed for carbaryl and 1-naphthol residues.

Animals↗
PubMedDate not supplied

Oxidation of pesticides by purified cytochrome P-450 isozymes from mouse liver.

5 cytochrome P-450 isozymes were purified from the livers of uninduced mice and reconstituted with purified NADPH cytochrome P-450 reductase and phospholipid. The pesticides parathion, fonofos, DEF, Mocap and profenofos were oxidized by the reconstituted monooxygenase system to form acetylcholinesterase (AChE) inhibitors. The bioactivation varied with the pesticide substrate and the cytochrome P-450 isozyme. Aldrin epoxidation occurred with all 5 isozymes, with cytochrome P-450 A1 being the most active. All fraction metabolized the pesticide synergist piperonyl butoxide (PBO) to form an inhibitory cytochrome P-450-PBO-metabolite complex. The reduced complex produced a spectrum in the Soret region which was characteristic for each of the cytochrome P-450 isozymes. Inhibition of aldrin epoxidation by PBO was found to be unrelated to the nature of the Soret spectrum.

Aldrin↗
PubMed1980

[Synergism of selected pesticides. 1. Acute oral toxicity in combined administration].

Comparative studies with male rats were performed to investigate the coergism of single oral doses of selected pesticides, the comparison being based on the lethal effects observed. The quantitative analysis of the dose-mortality relationship and the determination of the coergistic index evidenced a slight increase of the lethal effect with lindane-phosmet and lindane-carbaryl combinations. The combined administration of lindane and ethylenethiourea resulted in an additive lethal effect.

Animals↗
PubMed1978

Potentiation of methylmercury toxicity by piperonyl butoxide.

Methylmercury (MeHg) is an extremely potent neurotoxin about 25% of which is degraded in vivo to inorganic mercury. Piperonyl butoxide (PB) is a widely used pesticidal synergist which inhibits many mammalian detoxification reactions. In a preliminary experiment with the high doses of PB and MeHg, PB induced a 12% decrease in mean survival time and a 20% decrease in mean latency time to neurotoxicity. The weight loss in PB-MeHg group was far greater than the control MeHg group. In a dose response experiment, mean survival times in rats fed 40 ppm MeHg-C1 were 5.75, 5.3, and 5.0 weeks at 0, 0.5, and 1% PB, respectively. By the ninth week 25% of rats fed 20 ppm MeHg-C1 showed neurotoxicity and 63% of the 0.5% PB fed showed neurotoxicity with some mortality. In experiments at 20 ppm MeHg-C1 both PB fed groups weighted considerably less than corresponding controls.

Animals↗
PubMed1998

Mechanistic study on liver tumor promoting effects of piperonyl butoxide in rats.

Piperonyl butoxide, alpha-[2-(2-butoxyethoxy)ethoxy]-4,5-methylenedioxy-2-propyltol uene, is a widely used pesticide-synergist. Recently, results were reported indicating that piperonyl butoxide is a hepatocarcinogen in rat. Since the underlying mechanism was not elucidated, we examined the effects on rat liver cells in detail. For this purpose male F344 rats were administered piperonyl butoxide mixed in the diet at concentrations of 0 (negative control), 0.05, 0.2 or 2% for 2 days, 1, 2, and 4 weeks. As a positive control, phenobarbital was administered to rats for up to 4 weeks as a 0.1% solution in the drinking water. Increased liver weight, centrilobular hepatocellular hypertrophy due to increased smooth endoplasmic reticulum, decreased numbers and areas of connexin 32-positive spots per hepatocyte, and increased cell proliferation were observed in rats treated with 0.2 and 2% piperonyl butoxide. Similar results were obtained for 0.1% phenobarbital treated rats. Hepatocellular necrosis suggestive of hepatotoxicity was also observed in the 2% piperonyl butoxide group. These results indicate that the promoting mechanism of piperonyl butoxide in hepatocarcinogenesis is similar to that of phenobarbital, involving an ability to induce CYP isoenzymes and inhibit gap junctional intercellular communication. In addition, increased cell proliferation following hepatocellular necrosis may also play a role at high doses.

Animals↗
PubMed1992

The effect of pesticides on carp (Cyprinus carpio L). Acetylcholinesterase and its biochemical characterization.

The activity and molecular forms of acetylcholinesterase (AChE) were characterized in tissues of the carp (Cyprinus carpio). Tissue AChE activity was determined in response to specific inhibitors (ethopropazine, BW 284 C51) or pesticides (CuSO4, paraquat (PQ), methidathion (MD)). The highest AChE activity was found in the serum (878 +/- 100 U/liter), followed by the brain (113 +/- 12 U/liter), heart (89 +/- 6 U/liter), and trunk muscle (35 +/- 5 U/liter). Experiments with specific choline esterase inhibitors revealed a very low amount of pseudocholinesterase in all tissues studied. The ratio of the membrane-bound to the cytoplasmic-free AChE molecular forms was increased in the order of brain, trunk muscle, and heart. In sera of fish treated with MD (2 ppm) there was an 80% inhibition of AChE lasting for 2 weeks. Treatment with CuSO4 or PQ (both 5 ppm) led to a 50% decrease in the serum AChE activity followed by a transient increase over the control level. After 2 weeks of chronic treatment, AChE activity in fish exposed to CuSO4 returned to the control level, whereas in fish treated with PQ an elevated level (130% when compared to the control level) of enzyme activity was found. Our present experimental data indicate that pesticides occurring in natural waters not only inhibit AChE activity in fish but may influence the resynthesis of the enzyme as well.

Acetylcholinesterase↗
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↗
PubMed1992

Sub-acute toxicity of piperonyl butoxide in F344 rats.

Piperonyl butoxide, alpha-[2-(2-Butoxyethoxy)ethoxy]-4,5-methylenedioxy- 2-propyltoluene, is a pesticide synergist. F344 rats of both sex were maintained on diets containing 0, 0.6, 1.2 or 2.4% of piperonyl butoxide for 13 weeks. At the end of experimental period, they were necropsied. Selected organs were weighted and serum was analyzed by clinical chemistry. In male and female rats of the 2.4%-group, body weight gains were depressed, macroscopically, hepatomegaly was marked and liver weights were significantly higher than those of the control group. In male and female rats of all treated groups, relative kidney weights were significantly increased in a dose-dependent manner. Rats of the 2.4%-group had increased levels of albumin, cholesterol, urea nitrogen and gamma-glutamyl transpeptidase. Examination of livers of the male 2.4%-group by light microscopy showed enlarged hepatocytes with glassy cytoplasm and fatty deposition. On occasion, there was coagulative necrosis of a few hepatocytes in the periportal area and oval cell proliferation. The kidney of treated rats showed atrophy of epithelium in the proximal convoluted tubules. These results indicated that toxicity of piperonyl butoxide in rats was directed primarily to the liver and kidney.

Animals↗
PubMed1993

Subacute toxicity of piperonyl butoxide in ICR mice.

Piperonyl butoxide, alpha-[2-(2-butoxyethoxy)ethoxy]-4,5-methylenedioxy-2-propyltol uene, is a pesticide synergist. ICR mice of both sexes were maintained on diet containing 0, 0.1, 0.3 or 0.9% of piperonyl butoxide for 20 days. At the end of the experimental period, they were necropsied. Selected organs were weighed and serum chemistries were analyzed. In male and female mice of the 0.9% group, body weight, kidney and spleen weight were depressed in comparison to those of control group. Liver weight of the 0.3 and 0.9% group of both sexes were significantly higher than those of control group. Mice of the 0.9% group of both sexes had increased serum levels of cholesterol, total protein, gamma-glutamyl transpeptidase. Histological examination of livers from mice of the 0.9% group by light microscopy showed enlarged hepatocytes, anisonucleosis and single cell necrosis. The results indicated that subacute toxicity of piperonyl butoxide in ICR mice was directed primarily at liver.

Animals↗
PubMed1985

Effect of vitamin E and other amelioratory agents on the fenvalerate-mediated skin sensation.

Previous investigations have demonstrated that dermal exposure to fenvalerate or other synthetic pyrethroid insecticides can produce a skin sensory response characterized by an itching/tingling sensation in humans and animals. The objective of this investigation performed in guinea pigs was to establish treatments which would be effective against pyrethroid-mediated skin sensation. Two classes of agents were tested. Barrier agents, which block penetration of substances through the skin, did not significantly reduce the fenvalerate-mediated skin sensations. Post-treatments with steroidal Dermolate, antihistamine Delamine or anti-inflammatory aspirin did not significantly reduce the pyrethroid-mediated skin sensation. However, Bicozene (a local anesthetic cream) and Tashan (a vitamin A, D, and E-containing cream) were effective in reducing the pyrethroid-mediated skin sensations. Prior (30 min and 5h) dermal application of vitamin E was found to be effective in significantly reducing the fenvalerate-mediated skin sensation; even when applied 29 h prior to fenvalerate exposure, there appeared to be a reduced skin response. Piperonyl butoxide (PBO), a pesticide synergist, reduced the fenvalerate skin sensations when applied either directly to the skin or in conjunction with the pyrethroid.

Anesthetics, Local↗