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At least 19 recordsLinked to original sources
PubMed1992

Characterization of a carbofuran-degrading bacterium and investigation of the role of plasmids in catabolism of the insecticide carbofuran.

A bacterium capable of using the carbamate insecticide carbofuran as a sole source of carbon and energy, was isolated from soil. The ability to catabolise carbofuran phenol, produced by cleavage of the carbamate ester linkage of the insecticide, was lost at very high frequency when the bacterium was grown in the absence of carbofuran. Plasmid analyses together with curing and mating experiments indicated that the presence of a large plasmid (pIH3, greater than 199 kb) was required for the degradation of carbofuran phenol.

Biodegradation, Environmental↗
PubMed2004

In vitro metabolism of carbofuran by human, mouse, and rat cytochrome P450 and interactions with chlorpyrifos, testosterone, and estradiol.

Carbofuran is a carbamate pesticide used in agricultural practice throughout the world. Its effect as a pesticide is due to its ability to inhibit acetylcholinesterase activity. Though carbofuran has a long history of use, there is little information available with respect to its metabolic fate and disposition in mammals. The present study was designed to investigate the comparative in vitro metabolism of carbofuran from human, rat, and mouse liver microsomes (HLM, RLM, MLM, respectively), and characterize the specific enzymes involved in such metabolism, with particular reference to human metabolism. Carbofuran is metabolized by cytochrome P450 (CYP) leading to the production of one major ring oxidation metabolite, 3-hydroxycarbofuran, and two minor metabolites. The affinity of carbofuran for CYP enzymes involved in the oxidation to 3-hydroxycarbofuran is significantly less in HLM (Km=1.950 mM) than in RLM (Km=0.210 mM), or MLM (Km=0.550 mM). Intrinsic clearance rate calculations indicate that HLM are 14-fold less efficient in the metabolism of carbofuran to 3-hydroxycarbofuran than RLM or MLM. A screen of 15 major human CYP isoforms for metabolic ability with respect to carbofuran metabolism demonstrated that CYP3A4 is the major isoform responsible for carbofuran oxidation in humans. CYP1A2 and 2C19 are much less active while other human CYP isoforms have minimal or no activity toward carbofuran. In contrast with the human isoforms, members of the CYP2C family in rats are likely to have a primary role in carbofuran metabolism. Normalization of HLM data with the average levels of each CYP in native HLM, indicates that carbofuran metabolism is primarily mediated by CYP3A4 (percent total normalized rate (% TNR)=77.5), although CYP1A2 and 2C19 play ancillary roles (% TNR=9.0 and 6.0, respectively). This is substantiated by the fact that ketoconazole, a specific inhibitor of CYP3A4, is an excellent inhibitor of 3-hydroxycarbofuran formation in HLM (IC50: 0.31 microM). Chlorpyrifos, an irreversible non-competitive inhibitor of CYP3A4, inhibits the formation of 3-hydroxycarbofuran in HLM (IC50: 39 microM). The use of phenotyped HLM demonstrated that individuals with high levels of CYP3A4 have the greatest potential to metabolize carbofuran to its major metabolite. The variation in carbofuran metabolism among 17 single-donor HLM samples is over 5-fold and the best correlation between CYP isoform activity and carbofuran metabolism was observed with CYP3A4 (r2=0.96). The interaction of carbofuran and the endogenous CYP3A4 substrates, testosterone and estradiol, were also investigated. Testosterone metabolism was activated by carbofuran in HLM and CYP3A4, however, less activation was observed for carbofuran metabolism by testosterone in HLM and CYP3A4. No interactions between carbofuran and estradiol metabolism were observed.

Animals↗
PubMed2005

Carbofuran-induced neurochemical and neurobehavioral alterations in rats: attenuation by N-acetylcysteine.

Carbofuran, a widely used carbamate pesticide, has been reported to cause neurotoxicity. However, the underlying mechanisms involved in carbofuran neurotoxicity are not well understood. The present study was envisaged to investigate the possible role of oxidative stress in carbofuran neurotoxicity and to evaluate the protective effects of N-acetylcysteine (NAC). Acetylcholinesterase activity was significantly inhibited in all the regions of brain after carbofuran exposure (1 mg/kg body weight, orally, for 28 days). NAC, on the other hand, was found to partially restore the activity of acetylcholinesterase in carbofuran treated animals. Carbofuran exposure resulted in increased lipid peroxidation (LPO) in brain regions accompanied by decreased levels of glutathione. NAC administration to the carbofuran exposed animals lowered LPO along with partial repletion in glutathione levels. Concomitantly, the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase were significantly decreased after carbofuran exposure, while no significant change in the activity of glutathione-S-transferase was observed. NAC treatment to carbofuran treated rats resulted in protective effect on the activities of these enzymes. Marked impairment in the motor function was seen following carbofuran exposure, which is evident by significant decrease in the retention time of the rats on rotating rods. Cognitive deficits were also seen after carbofuran exposure as indicated by the significant decrease in active avoidance response. NAC treatment significantly improved the carbofuran-induced neurobehavioral deficits. The results clearly demonstrate that carbofuran exerts its neurotoxic effects by accentuating oxidative stress and suggest neuroprotective role of NAC in carbofuran neurotoxicity.

Acetylcholinesterase↗
PubMed1992

Characterization and growth response of bacteria in soil following application of carbofuran.

Enhanced biodegradation of carbofuran (2, 3-dihydro-2, 2 dimethyl-7-benzofuranyl methyl carbamate) is an economically significant, but poorly understood, microbial phenomenon in soil. A series of experiments was conducted to examine short term changes in soil bacterial populations stimulated by carbofuran application at field rates. In the field experiment, commercially formulated carbofuran and butylate (S-ethyl diisobutyl carbamothioate) were applied at 5.6 kg ai ha-1 and 8.4 kg ai ha-1, respectively, on a soil (Putnam silt loam) exhibiting enhanced degradation of carbofuran. In laboratory studies, technical grade carbofuran (20 mg kg-1 soil) was applied to samples of the field soil. Bacterial populations were estimated using non-selective (tryptic soy agar) and selective media containing carbofuran or butylate. Largest population increases in pesticide-treated soil were observed between 7 and 15 days after treatment (DAT) compared to populations in non-treated soil. Significant increases (P less than 0.05) in total bacterial populations and presumed carbofuran-degraders due to carbofuran application were associated with increased populations of Pseudomonas spp. and Flavobacterium spp. Application of carbofuran appeared to provide a competitive advantage to these species over actinomycetes persisting beyond 20 DAT. Growth responses of bacteria to carbofuran in the Putnam soil were compared to those in a native prairie soil (Mexico silt loam), which exhibited a much slower rate of carbofuran degradation. Bacterial population response to carbofuran was measurable, but small and short-lived. Perpetuation of the enhanced degradation phenomenon may lie in a persistent pesticide-induced competitive advantage given to a very small segment of the microbial population. This advantage may not be detectable after 20 days using conventional plating techniques.

Bacteria↗
PubMed1994

Carbofuran-degrading bacteria from previously treated field soils.

Laboratory incubation studies were made on soils collected from five field sites with different histories of treatment with carbofuran. All soils treated earlier with carbofuran degraded the compound more rapidly than untreated samples of the same soils. Reduced rates of degradation in the presence of chloramphenicol imply that soil bacteria are primarily responsible for the breakdown of carbofuran in these soils. Sixty-eight bacteria, capable of degrading carbofuran as the sole source of carbon and nitrogen, were isolated from liquid cultures of treated soils. The concentration of carbofuran in the liquid medium used for isolation and subsequent culture of carbofuran-degrading isolates appeared to affect the stability of their ability to degrade. Similar types of carbofuran-degrading bacteria were isolated from different soils and several different types were isolated from one soil. All carbofuran-degrading isolates were Gram-negative, aerobic rods which hydrolysed the insecticide to carbofuran phenol. They were separated into four groups on the basis of a limited number of phenotypic characters. There was a good correlation between the phenotype of carbofuran-degrading isolates and the stability of their ability to degrade. Fourteen isolates were placed in phenotypic group I and 13 of these did not degrade carbofuran after one subculture in liquid medium. Phenotypic groups II, III and IV consisted of 54 isolates in total (3, 46 and 5 isolates respectively) and 52 of these retained their ability to degrade carbofuran when subcultured.

Biodegradation, Environmental↗
PubMed2001

The effect of initial concentration of carbofuran on the development and stability of its enhanced biodegradation in top-soil and sub-soil.

Carbofuran was incubated in top-soil and sub-soil samples from a pesticide-free site at a range of initial concentrations from 0.1 to 10 mg kg-1. Amounts of the incubated soils were removed at intervals over the subsequent 12 months, and the rate of degradation of a second carbofuran dose at 10 mg kg-1 was assessed. An applied concentration as low as 0.1 mg kg-1 to top-soil resulted in more rapid degradation of the fresh addition of carbofuran for at least 12 months. The degree of enhancement was generally more pronounced with the higher initial concentrations. When the same study was conducted in sub-soil samples from the same site, an initial dose of carbofuran at 0.1 mg kg-1 resulted in only small increases in rates of degradation of a second carbofuran dose. However, degradation rates in the sub-soil samples were, in many instances, considerably greater than in the corresponding top-soil samples, irrespective of pre-treatment concentration or pre-incubated period. Initial doses of 0.5 mg kg-1 and higher applied to sub-soil successfully activated the sub-soil microflora. Application of the VARLEACH model to simulate carbofuran movement through the soil profile indicated that approximately 0.01 mg kg-1 of carbofuran may reach a depth of 70 cm 400 days after a standard field application. The results therefore imply that adaptation of the sub-soil microflora (c 1 m depth) by normal field rate applications of carbofuran is unlikely to occur. In experiments to investigate this in soils exposed to carbofuran in the field, there was no apparent relationship between top-soil exposure and degradation rates in the corresponding sub-soils. The results further confirmed that same sub-soil samples have an inherent capacity for rapid biodegradation of carbofuran. The high levels of variability observed between replicates in some of the sub-soil samples were attributed to the uneven distribution of a low population of carbofuran-degrading micro-organisms in sub-surface soil. There was no apparent relationship between soil microbial biomass and degradation rates within or between top-soil and sub-soil samples.

Bacteria↗
PubMed2004

Sphingomonas sp. strain SB5 degrades carbofuran to a new metabolite by hydrolysis at the furanyl ring.

Microorganisms capable of degrading carbofuran were isolated from soils and examined for the degradation of this pesticide at ring structure. An isolate that could degrade carbofuran and carbofuran-7-phenol was selected for further studies. The 16S rRNA analysis results showed that the isolate belongs to the genus of Sphingomonas, close to dioxin and dicamba degraders, and is named Sphingomonas sp. SB5. SB5 did not show any similarity of 16S rRNA to known carbofuran degraders. When time-course degradation of carbofuran by SB5 was examined by solvent extraction combined with liquid chromatographic analysis, almost complete disappearance of carbofuran was observed within 12 h, giving several accumulative metabolites. Bacterial cultures incubated with carbofuran-7-phenol suggested that the accumulated metabolites were derived from carbofuran-7-phenol. The control without SB5 and kanamycin-treated SB5 did not show any metabolite, suggesting a biological involvement in the degradation of carbofuran. GC/MS and LC/MS analyses identified 2-hydroxy-3-(3-methylpropan-2-ol) phenol as one of the accumulated metabolites, suggesting that the strain SB5 could degrade carbofuran-7-phenol by hydrolysis at the furanyl ring. This is the first report to identify 2-hydroxy-3-(3-methylpropan-2-ol) phenol as a new product derived biologically from carbofuran-7-phenol.

Carbofuran↗
PubMed2006

Degradation of carbofuran in water by solar photocatalysis in presence of photosensitizers.

The effect of the presence of photosensitizers, methylene blue (MB) and rose Bengal (RB), on the degradation of carbofuran (2,3-dihydro-2,2-dimethylbenzofuran-7-yl methylcarbamate) in water in a solar photocatalytic system was investigated. It was found that as compared to MB, RB generally showed a stronger effect on the decomposition of carbofuran under comparable conditions. Among the conditions studied, adding 2 x 10(-6) M of RB, that corresponding to 2% of the initial concentration of carbofuran solution in the system, rendered the most effective degradation of carbofuran. As a result, a carbofuran removal percentage of 69.9%, a mineralization efficiency of 28.0%, and a microtoxicity reduction of 65.0% could be achieved. The degradation and mineralization of carbofuran was found to follow the pseudo-first order reaction kinetics. The decomposition mechanism of carbofuran was further investigated through identification of the intermediates to elaborate the influence of dye photosensitizer on the solar photocatalysis of carbofuran in water. On the basis of the intermediates identified, including carbofuran phenol, 3-hydroxy carbofuran phenol, and substituted alcohols (3-phenoxy 1-propanol, 2-ethyl 1-hexanol, 2-butoxyl ethanol), it appears that hydrolysis and hydroxylation were the two key mechanisms for decomposing carbofuran during the process of solar photocatalysis with the aid of dye photosensitizer.

Biodegradation, Environmental↗
PubMed1996

Behavioral effects of waterborne carbofuran in goldfish.

The effects of concentration (1, 10, 100 microg/L) and duration (4, 8, 12 h) of exposure to carbofuran were assessed on the swimming activity, social interactions, and behavioral responses of goldfish to a flow (0.1 L/min) of water, with or without chironomids. Observations were also made on the behavioral responses of unexposed goldfish to a flow (0.1 L/min) of carbofuran-contaminated water. A 4-h exposure of goldfish 1 microg/L carbofuran produced a significant increase in sheltering, burst swimming, and nipping. Responses were enhanced at 100 microg/L. After a 12-h exposure, the behavioral effects of 1 microg/L carbofuran were less apparent. However, burst swimming at 10 microg/L, and sheltering, nipping and burst swimming at 100 microg/L, were still significantly increased after a 12-h exposure to carbofuran. Grouping was not consistently affected by exposure conditions. Chemical attraction to a filtrate of chironomids was significantly reduced after the 4-h exposure to 1 microg/L carbofuran. Decreased attraction to the food extract was less apparent after the 12-h exposure, except at 100 microg/L carbofuran. A significant decrease in attraction to a flow of uncontaminated water was also observed after a 4-h exposure to 10 and 100 microg/L carbofuran. Unexposed goldfish did not show avoidance reaction to a flow of carbofuran-contaminated water, even at a concentration (10 mg/L) exceeding the mean 96-h LC-50 in cyprinids (0.5-1 mg/L). However, at all concentrations tested (0.1, 1, 10 mg/L), goldfish quickly reacted to the introduction of the solution of carbofuran by increased burst swimming and nipping. These results are discussed in the light of the data concerning behavioral and neurotoxic effects of carbamate and organophosphorous insecticides in fish.

Animals↗
PubMed2006

N-acetylcysteine ameliorates carbofuran-induced alterations in lipid composition and activity of membrane bound enzymes.

The present work investigates the protective effects of N-acetylcysteine (NAC) on carbofuran-induced alterations in lipid composition and activity of membrane bound enzymes (Na+-K+-ATPase and Ca2+-ATPase) in the rat brain. Animals were exposed to carbofuran at a dose of 1 mg/kg body weight, orally, for a period of 28 days. A significant increase in lipid peroxidation in terms of TBARS was observed in brain after carbofuran exposure. NAC administration (200 mg/kg body weight) on the other hand lowered the carbofuran-induced lipid peroxidation to near normal. The increased lipid peroxidation following carbofuran exposure was accompanied by a significant decrease in the levels of total lipids, which is attributed to the reduction in phospholipid levels. Furthermore, NAC administration had a beneficial effect on carbofuran-induced alterations in lipid composition. The ratio of cholesterol to phospholipid, a major determinant of membrane fluidity, was increased in response to carbofuran exposure. This was associated with decreased activity of Na+-K+-ATPase and Ca2+-ATPase. NAC was observed to offer protection by restoring the cholesterol to phospholipid ratio along with the activity of Na+-K+-ATPase and Ca2+-ATPase. The results clearly suggest that carbofuran exerts its neurotoxic effects by increasing lipid peroxidation, altering lipid composition and activity of membrane bound enzymes. NAC administration ameliorated the effects of carbofuran suggesting its potential therapeutic effects in carbofuran neurotoxicity.

Acetylcysteine↗
PubMed2001

Carbofuran suppresses T-cell-mediated immune responses by the suppression of T-cell responsiveness, the differential inhibition of cytokine production, and NO production in macrophages.

The effects of carbofuran (2,3-dihydro-2,2-dimethyl-7-benzo-furanol N-methylcarbamate) on the functions of T cells in splenocytes and peritoneal macrophages were examined in view of T-cell-mediated immune response (CMIR) in male C57BL/6 mice. Intraperitoneal administration of carbofuran (0.075, 0.15 and 0.3 mg/kg body weight) resulted in significant suppression of delayed type hypersensitivity (DTH), indicating that it caused the suppression of CMIR. Carbofuran decreased Concanavalin A (Con A)- and alloantigen-induced proliferation, and interleukin (IL)-2 production of splenocytes. In vitro addition of rIL-2 could not completely restore the suppressed T-cell proliferation, and IL-2-induced proliferation of Con A-activated splenocytes was also suppressed, which implied that carbofuran caused defects in IL-2 production and responsiveness of splenocytes to IL-2, leading to the suppression of T-cell proliferation. Con A-induced production of interferon-gamma (IFN-gamma) was significantly suppressed by carbofuran, while that of IL-4 was not affected. The production of transforming growth factor-beta from splenocytes was also significantly inhibited by carbofuran. Judging from these results, carbofuran might directly suppress the cytokine production in T helper 1 (Th1) cells. In addition, IFN-gamma-induced production of nitric oxide (NO) in macrophages was also inhibited by carbofuran, which might be one of the important mechanisms of carbofuran-induced CMIR suppression in mice. Collectively, the present study suggests that carbofuran might suppress CMIR through the suppression of T-cell responsiveness, IFN-gamma production in Th1 cells, and NO generation in macrophages.

Animals↗
PubMed1989

Concerted role of carboxylesterases in the potentiation of carbofuran toxicity by iso-OMPA pretreatment.

Pretreatment of rats with the nonspecific esterase inhibitor iso-OMPA (1 mg/kg sc) 1 h prior to carbofuran (2,3-dihydro-2,2-dimethyl-7-benzofuranyl N-methylcarbamate, 0.5 mg/kg sc) administration potentiated carbofuran toxicity by more than threefold. Neither iso-OMPA nor carbofuran in the given doses produced any gross toxic signs. Rats receiving combined treatment, however, showed severe hypercholinergic signs (salivation, tremors, muscle fasciculations, and convulsions) within 5-10 min following carbofuran administration, and the severity was comparatively greater than that observed with an acute dose of carbofuran (1.5 mg/kg sc). Rats pretreated with iso-OMPA (0.5 mg/kg) died within 10-15 min following the acute dose of carbofuran (1.5 mg/kg). Each drug when given alone (1.0 mg/kg iso-OMPA, 0.5 mg/kg carbofuran) caused a significant (p less than .01) inhibition of carboxylesterase (CarbE) activity in brain structures (cortex, stem, striatum, and hippocampus), skeletal muscle (hemidiaphragm), liver, and plasma, whereas acetylcholinesterase (AChE) activity remained significantly (p greater than .01) unchanged. The maximal CarbE inactivation in plasma (less than 14% remaining activity) following either drug indicated a tremendous nonspecific binding to non-AChE serine-containing enzymes. iso-OMPA pretreatment markedly potentiated carbofuran's anticholinesterase activity both in neuronal and in nonneuronal tissues. It can be concluded that iso-OMPA pretreatment potentiates carbofuran toxicity either by preventing nonspecific binding of carbofuran to CarbE and/or possibly by inhibiting its detoxification.

Animals↗
PubMed1994

Carbofuran toxicity.

Carbofuran, an anticholinesterase carbamate, is commonly used as an insecticide, nematicide, and acaricide in agricultural practice throughout the world. Due to its widespread use in agriculture, contamination of food, water, and air has become imminent, and consequently adverse health effects are inevitable in humans, animals, wildlife, and fish. Currently, carbofuran's involvement is most frequently encountered in malicious poisoning. The literature on chemical properties, acute toxicity data, poisoning incidences, pharmacokinetics, and mechanism of toxicity of carbofuran is briefly reviewed. Much emphasis is given to the metabolism of carbofuran, and the impact of carbofuran and its two major metabolites (3-hydroxycarbofuran and 3-ketocarbofuran) on overall toxicity. Biochemical (cholinergic and noncholinergic), hematological, and immunological effects induced by carbofuran are discussed in detail. Carbofuran and/or its major metabolites can cross the placental barrier and produce serious effects on the maternal-placental-fetal unit. Carbofuran's toxicity can be potentiated by simultaneous exposure with other cholinesterase inhibitors. Literature on various biomarkers of carbofuran exposure and on induced adverse health effects is also presented. To date, a combination of atropine and memantine remains the most effective antidotal treatment against acute carbofuran toxicity.

Agricultural Workers' Diseases↗
PubMed2003

Influence of suspended solids on acute toxicity of carbofuran to Daphnia magna: I. Interactive effects.

This study explored the effects on Daphnia magna from exposure to the pesticide carbofuran in combination with stress from suspended solids exposure. Our objective was to assess whether suspended solids affects the toxicodynamic response of D. magna to carbofuran. A series of laboratory experiments was performed where animals were exposed to carbofuran concentrations ranging from 0 to 160 microg/l in combination with suspended solids concentrations ranging from 0 to 10000 mg/l. In the absence of suspended solids, effects of carbofuran were dose dependent and resulted in an EC(50) of 92 microg/l. Exposure to suspended solids, up to extreme levels that may be encountered in the environment and in the absence of carbofuran, showed no measurable toxicity. When D. magna were exposed to a constant carbofuran concentration, the numbers of affected organisms increased with increasing suspended solids concentrations. At a suspended solids concentration of 1000 mg/l, the EC(50) for carbofuran was reduced by half to 45 microg/l. The relationship between the toxicity of carbofuran (microg/l) and the concentration of suspended solids (mg/l) can be described with the following equation: carbofuran EC(50)=72 exp(-0.00014 [suspended solids]). An analysis of the data indicates that this relationship is consistent with a potentiated toxicity mechanism rather than an additive model.

Animals↗
PubMed2004

Nanocolloidal gold-based immunoassay for the detection of the N-methylcarbamate pesticide carbofuran.

Nanocolloidal gold particles were prepared and labeled to an anti-carbofuran monoclonal antibody (Mab). This conjugate was dispensed on the conjugated pad of a porous glass fiber. Ovalbumin (OVA)-carbofuran and goat anti-mouse IgG were dispensed on the nitrocellulose (NC) membrane and served as the test line and control line, respectively. The carbofuran-containing sample migrated to the NC membrane and reacted with the anti-carbofuran Mab labeled with the colloidal gold. The mixture diffused along the membrane and passed through the OVA-carbofuran in the test line via capillary action. The more analyte present in the sample, the more effectively it will compete with the carbofuran immobilized on the test line for binding to the limited amount of antibody labeled with colloidal gold. An adequate amount of carbofuran could prevent attachment of the colored conjugate to the test line. The presence or absence of a colored band on the test line could indicate a negative or positive result, respectively. When measured to the water sample spiked with carbofuran, this was obtained at or above 0.25 mg/L of carbofuran. The major advantages of the one-step strip test are that the detection time needed was <10 min and all of the reagents are included in the test device.

Antibodies, Monoclonal↗
PubMed2005

Occupational exposure to carbofuran and the incidence of cancer in the Agricultural Health Study.

Carbofuran is a carbamate insecticide registered for use on a variety of food crops including corn, alfalfa, rice, and tobacco. An estimated 5 million pounds of carbofuran is used annually in the United States, and 45% of urban African-American women have detectable levels of carbofuran in their plasma. Nitrosated carbofuran has demonstrated mutagenic properties. We examined exposure to carbofuran and several tumor sites among 49,877 licensed pesticide applicators from Iowa and North Carolina enrolled in the Agricultural Health Study. We obtained information regarding years of use, frequency of use in an average year, and when use began for 22 pesticides using self-administered questionnaires. Poisson regression was used to calculate rate ratios (RR) and 95% confidence intervals (CIs) adjusting for potential confounders. Lung cancer risk was 3-fold higher for those with > 109 days of lifetime exposure to carbofuran (RR = 3.05; 95% CI, 0.94-9.87) compared with those with < 9 lifetime exposure days, with a significant dose-response trend for both days of use per year and total years of use. However, carbofuran use was not associated with lung cancer risk when nonexposed persons were used as the referent. In addition, carbofuran exposure was not associated with any other cancer site examined. Although carbamate pesticides are suspected human carcinogens, these results should be interpreted cautiously because there was no a priori hypothesis specifically linking carbofuran to lung cancer.

Adult↗