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PubMed1979

A seasonal comparison of parathion degradation on oranges in Arizona.

A study comparing the leaf residue decay of parathion wettable powder (8 lbs per acre) on oranges was carried out on neighboring plots in Arizona beginning in October, 1975, and February, 1976. While identical amounts of parathion were present immediately after spraying and the half-life of parathion was the same in both months, there was, on the average, more parathion residue during February. Graphs of parathion and paraoxon levels over time differed between months (in excess of sampling variability). This most likely was due to the daily influences of climatological variables which were obviously different in October and February.

Arizona↗
PubMed1975

Persistence of parathion and its oxidation to paraoxon on the soil surface as related to worker reentry into treated crops.

Soil and dust samples from beneath citrus trees contained relatively high concentrations of paraoxon and parathion for at least 45 days after parathion was applied at normal rates. These data indicate that parathion dripping on dry soil from sprayed crops, or sprayed directly on the soil surface, can persist for long periods and be oxidized to the highly toxic paraoxon. The residue concentrations are much higher on the loose dust particles than in the bulk soil. The data indicate that the soil or grove floor should be considered as a possible contributing source of toxicant along with foliage, or dust on foliage, to workers reentering treated fields. In any event, the data confirmed the high rates of oxidation of parathion to paraoxon on particulate matter, whether on foliage (SPEAR et al., 1974) or at the soil surface. The particulate matter appears to contribute to the accumulation of paraoxon, either by enhancing oxidation of parathion to paraoxon or by decreasing dissipation of paraoxon.

Agricultural Workers' Diseases↗
PubMed1987

Intrinsic metabolic clearance of parathion and paraoxon by livers from fish and rodents.

The specific activities of hepatic enzymes involved in both the activation and detoxification of the anticholinesterase insecticide parathion were significantly greater in both rats and mice compared to either fathead minnows or rainbow trout. Whereas the rates of parathion desulfuration and hydrolysis were comparable, the specific activity for paraoxon hydrolysis was approximately threefold greater than its rate of formation for all species except trout. The kinetic data, however, indicate that the significantly greater Km for paraoxon hydrolysis limits its detoxification. Accordingly, the data are consistent with the progressive accumulation of this toxic metabolite in liver tissue incubated in vitro with parathion. The similar Km for parathion desulfuration and hydrolysis by rodents is consistent with the proposed mechanism of catalysis involving a common S-oxide intermediate. Due to the slow rates of enzyme catalysis, reliable kinetic estimates for the hydrolytic reactions were not possible for both species of fish. Assuming comparable Km values for paraoxon hydrolysis in rodents and fish, the net accumulation of paraoxon in tissue water may be quite similar between species and metabolic transformation may not be an important determinant of the species-selective toxicity of parathion.

Animals↗
PubMed1991

Percutaneous absorption of parathion in vitro in porcine skin: effects of dose, temperature, humidity, and perfusate composition on absorptive flux.

The effect of environmental factors on the percutaneous absorption of parathion in excised porcine skin was assessed in a flow-through diffusion cell system by varying the temperature (T), relative humidity (%RH), perfusate flow rate (F), and composition (porcine serum) at three parathion doses (4, 40, and 400 micrograms/cm2) compared to standard conditions (air temperature = 37 degrees C, perfusate temperature = 37 degrees C, %RH = 60, flow rate = 4 ml/hr, and standard bovine serum albumin medium). Parathion absorption was assessed by monitoring total radiolabeled activity appearing in the perfusate over time. High relative humidity significantly increased parathion penetration, as did two elevated temperature conditions. The effects of flow rate and perfusate composition were variable and dose dependent. In the present studies, lower applied doses appeared to be more sensitive to changes in the environmental conditions studied. These results suggest that these parameters have independent and different degrees of effect on parathion percutaneous absorption. Experimental conditions should be strictly controlled and dose-response studies need to be conducted when evaluating transdermal studies. Finally, if similar effects occur in vivo, the risk assessment calculations on percutaneous absorption should take these parameters into consideration.

Animals↗
PubMed1991

Parathion (O,O-dimethyl-O-p-nitrophenyl phosphorothioate) induces pineal melatonin synthesis at night.

The effects of parathion on male rat pineal N-acetyltransferase (NAT) activity, hydroxyindole-O-methyltransferase (HIOMT) activity and pineal and serum melatonin levels at the end of light period (2000 h) and at night (2300 h and 0100 h) were studied. Additionally, pineal levels of 5-hydroxytryptophan (5-HTP), serotonin (5-HT), and 5-hydroxyindole acetic acid (5-HIAA) were estimated. Parathion was administered intragastrically at total doses (over 6 days) of either 6.5 or 13 mg/kg. Control rats received vehicle (corn oil) only. During the study, the rats were exposed to light:dark cycles of 14:10 with light off at 2100 h. Pineal NAT activity was increased at 0100 h following parathion administration at both doses, but HIOMT activity was unaffected. Pineal and serum melatonin levels were increased at night (2300 h and 0100 h) after the 13 mg/kg dose of parathion while the lower dose increased pineal melatonin only at 0100 h. Also, both doses decreased 5-HTP at 2000 h while the lower dose increased it at 2300; 5-HT was significantly decreased at 2300 h and 5-HIAA levels were lower but only significantly so for the 13 mg/kg dose at 2000 h. The results indicate that parathion has significant effects on pineal melatonin synthesis by mechanisms which remain unknown.

Acetylserotonin O-Methyltransferase↗
PubMed1991

The effect of glutathione monoethyl ester on the potentiation of the acute toxicity of methyl parathion, methyl paraoxon or fenitrothion by diethyl maleate in the mouse.

Depletion of hepatic glutathione in the mouse by pretreatment with diethyl maleate (DEM) is known to potentiate the acute toxicities of many dimethyl-substituted organothiophosphate insecticides. However, certain studies have raised doubts regarding the participation of glutathione in the detoxification of methyl parathion in the mouse, and hence the putative mechanism of action of DEM-induced potentiation of this insecticide. The present study evaluates the hypothesis that DEM potentiates the acute toxicities of methyl parathion, methyl paraoxon, and fenitrothion by a mechanism other than glutathione depletion. One hour following pretreatment of mice with DEM (0.75 ml/kg i.p.), glutathione was markedly depleted and the acute toxicities of methyl parathion, methyl paraoxon and fenitrothion were potentiated. Administration of glutathione monoethyl ester (20 mmol/kg p.o.) to DEM-pretreated mice attenuated DEM-depletion of hepatic glutathione, or maintained glutathione at or above control levels. However, glutathione monoethyl ester did not alter the DEM-induced potentiation of the lethality of these insecticides. Furthermore, administration of glutathione monoethyl ester to naive mice increased hepatic glutathione levels, but did not affect the percentage of animals succumbing to a challenge dose of methyl parathion, methyl paraoxon, or fenitrothion. These data indicate that DEM potentiates the toxicity of methyl parathion, methyl paraoxon or fenitrothion by a mechanism unrelated to hepatic glutathione content.

Animals↗
PubMed2005

Plasmid-borne catabolism of methyl parathion and p-nitrophenol in Pseudomonas sp. strain WBC-3.

Pseudomonas sp. strain WBC-3 utilises methyl parathion (MP) or p-nitrophenol (PNP) as the sole source of carbon, nitrogen, and energy. A plasmid designated pZWL0 of approximately 70 kb in this strain was found to be responsible for MP and PNP degradation. This was based on the fact that the plasmid-cured strains showed PNP- MP- phenotype and the PNP+ MP+ phenotype could be conjugally transferred. We have also cloned a 3.4-kb HindIII fragment which exhibited methyl parathion hydrolase activity, which revealed a methyl parathion hydrolase (mph) gene whose DNA sequence is 99.5% identical to the recently identified mpd gene from Plesiomonas sp. M6 [C. Zhongli, L. Shunpeng, F. Guoping, Isolation of methyl parathion-degrading strain M6 and cloning of the methyl parathion hydrolase gene, Appl. Environ. Microbiol. 67 (2001) 4922-4925]. The mph gene was functionally expressed in Escherichia coli and the relative activities of the enzyme against different substrates were determined. The sequence alignment and phylogenetic analysis suggested that MPH and MPD evolved independently from other well-studied organophosphate hydrolases and may be originated from class B beta-lactamase family. Subsequently obtained a 6.5-kb KpnI and BamHI fragment containing the above HindIII fragment revealed that the mph gene was physically located in a typical transposon.

Amino Acid Sequence↗
PubMed2005

Optical microbial biosensor for detection of methyl parathion pesticide using Flavobacterium sp. whole cells adsorbed on glass fiber filters as disposable biocomponent.

An optical microbial biosensor was described for the detection of methyl parathion pesticide. Whole cells of Flavobacterium sp. were immobilized by trapping in glass fiber filter and were used as biocomponent along with optic fiber system. Flavobacterium sp. has the organophosphorus hydrolase enzyme, which hydrolyzes the methyl parathion into detectable product p-nitrophenol. The immobilized microbial biocomponent was disposable, cost-effective and showed high reproducibility and uniformity. The detection of methyl parathion by the use of disposable microbial biocomponent with optical biosensor was simple, single step and direct measurement of very low quantity of the sample. The home made reaction vessel was small and needed only 75 microl of sample. A lower detection limit 0.3 microM methyl parathion was estimated from the linear range (4-80 microM) of calibration plot of organophosphorus hydrolase enzymatic assay. The applicability to synthetic methyl parathion spiked samples was demonstrated.

Aryldialkylphosphatase↗
PubMed2005

Evaluation of the susceptibility of the cultured shrimp Litopenaeus vannamei to vibriosis when orally exposed to the insecticide methyl parathion.

The causes of disease in cultured shrimp are difficult to ascertain but there is evidence that disease is correlated with environmental factors. Crustaceans are particularly sensitive to insecticides due to their close phylogenetic relationship with insects. The objective of this study was to investigate whether there was an increased susceptibility of the shrimp Litopenaeus vannamei to Vibrio parahaemolyticus, when exposed to methyl parathion. The outline of the study was the following: An LC50 96 h was determined to methyl parathion orally offered to juvenile shrimp. Further experiments were carried out in order to determine a concentration that affected the shrimp (verified by measuring the acethylcholinesterase activity) while producing minimal mortalities. This sublethal concentration was used in a susceptibility experiment where methyl parathion was offered to shrimp which were later injected with V. parahaemolyticus in a dose expected to kill less than 15%. Probit analysis estimated a 96 h median lethal concentration (LC50) of 1.56 microg g(-1). Mortality and AChE activity showed a concentration-response relationship in the exposure treatments. The median inhibitory concentration (IC50) determined was 0.029 microg g(-1). These results suggested that a concentration of 0.1 microg g(-1) was appropriate for the bacteria-pesticide interaction test as it was able to elicit 11.1% mortality after 10 days of exposure, while producing an AChE inhibition of 57.12%. Cumulative mortalities were significantly increased (P<0.01) in the treatment that combined exposure to methyl parathion and V. parahaemolyticus (35.19%) in comparison with methyl parathion or V. parahaemolyticus alone (9.26% and 7.41%, respectively).

Acetylcholinesterase↗
PubMed2005

Degradation mechanism and the toxicity assessment in TiO2 photocatalysis and photolysis of parathion.

The photocatalytic degradation of methyl parathion was carried out using a circulating TiO2/UV reactor. The experimental results showed that parathion was more effectively degraded in the photocatalytic condition than the photolysis and TiO2-only condition. With photocatalysis, 10mg/l parathion was completely degraded within 60 min with a TOC decrease exceeding 90% after 150 min. The main ionic byproducts during photocatalysis were measured. The nitrogen from parathion was recovered mainly as NO3-, NO2- and NH4+, 80% of the sulfur as SO4(2-), and less than 5% of the phosphorus as PO4(3-). The organic intermediates 4-nitrophenol and paraoxon were also identified, and these were further degraded. Two different bioassays (Vibrio fischeri and Daphnia magna) were used to test the acute toxicity of solutions treated by photocatalysis and photolysis. A Microtox test using V. fischeri showed that the toxicity, expressed as the relative toxicity (%), was reduced almost completely after 90 min under photocatalysis, whereas only an 83% reduction was achieved with photolysis alone. Another toxicity test using D. magna also showed that the relative toxicity disappeared after 90 min under photocatalysis, whereas there was a 65% reduction in relative toxicity with photolysis alone. The pattern of toxicity reduction parallels the decrease in parathion and TOC concentrations.

Aliivibrio fischeri↗
PubMed2006

The partitioning and modelling of pesticide parathion in a surfactant-assisted soil-washing system.

Soil sorption of organic pollutants has long been a problematic in the soil washing process because of its durability and low water solubility. This paper discussed the soil washing phenomena over a wide range of parathion concentrations and several soil samples at various fractions of organic content (foc) levels. When parathion dosage is set below the water solubility, washing performance is stable for surfactant concentrations above critical micelle concentration (cmc) and it is observed that more than 90% of parathion can be washed out when dosage is five times lower than the solubility limit. However, such trends change when non-aqueous phase liquids (NAPL) is present in the system. Parathion extraction depends very much on the surfactant dosage but is not affected by the levels of foc in the system. In between the extreme parathion dosage, a two-stage pattern is observed in these boundary regions. Washing performance is first increased with additional surfactant, but the increase slows down gradually since the sorption sites are believed to be saturated by the huge amount of surfactant in the system. A mathematical model has included foc to demonstrate such behavior and this can be used as a prediction for extraction.

Adsorption↗
PubMed2006

Effects of methyl parathion on Chasmagnathus granulatus hepatopancreas: protective role of sesamol.

The protective role of sesamol, an inhibitor of the mixed function oxygenase (MFO) system, against histopathological effects of methyl parathion in the hepatopancreas of the estuarine crab, Chasmagnathus granulatus, was studied. Exposure (72 h) to a sublethal dose (0.05 mg/kg/day; 10% of 72 h-LD50) of injected methyl parathion increased the percentage of damaged hepatopancreatic tubules. Presence of melanin-like deposits in the connective tissue between hepatopancreatic tubules was also observed. Antioxidant enzyme activities (catalase and glutathione S-transferase) and lipid peroxidation (LPO) levels were also increased in hepatopancreas of crabs injected with methyl parathion. Pretreatment with sesamol (0.85 mg/kg/day) significantly protected against all these effects. These findings suggest that the hepatopancreatic damages induced by methyl parathion are due to LPO of hepatopancreatocytes membranes, as a consequence of the oxidative stress generated after methyl parathion oxidative biotransformation mediated by the MFO system.

Animals↗
PubMed2006

Diazinon, chlorpyrifos and parathion are metabolised by multiple cytochromes P450 in human liver.

This research describes both the activation and detoxification of diazinon, chlorpyrifos and parathion by recombinant P450 isozymes and by human liver microsomes that had been characterised for P450 marker activities. Wide variations in activity were found for diazinon (50 microM; 500 microM) activation to diazoxon, chlorpyrifos (100 microM) to chlorpyrifos oxon and parathion (5 microM, 20 microM and 200 microM) to paraoxon in NADPH-dependent reactions. In parallel, the dearylated metabolites pyrimidinol (IHMP), trichloro-2-pyridinol (TCP) and p-nitrophenol (PNP) were produced from diazinon, chlorpyrifos and parathion, respectively, with similarly wide variations in activity. There were significant correlations between diazoxon formation from diazinon (50 microM; 500 microM) with the three CYP3A4/5 marker reactions, while IHMP formation correlated significantly with the three CYP3A4/5 reactions, the CYP2C8 marker reaction (p<0.05) and the CYP2C19 marker (p<0.01). Chlorpyrifos oxon formation from chlorpyrifos did not correlate with any of the P450 markers but TCP formation correlated with one of the CYP3A4/5 reactions (p<0.01) and CYP2C8 (p<0.01), CYP2C19 (p<0.01) and CYP1A2 (p<0.01) mediated reactions. There were significant relationships between paraoxon formation from parathion (5 microM, 20 microM and 200 microM) and the CYP3A4/5, CYP2C8 and CYP1A2 mediated reactions, although only the latter two isoforms correlated significantly with the lowest parathion concentration. Recombinant CYPs 2D6, 2C19, 3A5, 3A4 were most efficient in producing diazoxon and IHMP from diazinon; CYPs 2D6, 3A5, 2B6 and 3A4 were best at producing chlorpyrifos-oxon and CYPs 2C19, 2D6, 3A5 and 3A4 at producing TCP from chlorpyrifos (100 microM). These data strongly suggest that CYPs 3A4/5, 2C8, 1A2, 2C19 and 2D6 are primarily involved in the metabolism of all three OPs, although the profile of participating isoforms was different for each of the pesticides suggesting that chemical structure influences which P450s mediate the reaction. The marked inter-individual variation in expression of the various P450 isozymes may result in sub-populations of individuals that produce higher systemic oxon levels with increased susceptibility to OP toxicity.

Chlorpyrifos↗
PubMedDate not supplied

Inhibition of ovarian compensatory hypertrophy by the administration of methyl parathion in hemicastrated albino rats.

Methyl parathion, an organophosphorus pesticide that is a potent acetylcholinesterase inhibitor in animals, was administered IP in graded doses from 2.5 to 5.0 mg/kg body weight to normal hemicastrated virgin rats for 15 consecutive days. Sham-operated and hemicastrated control groups were treated with a similar quantity of olive oil vehicle. The vaginal smears and body weights of treated and control groups were recorded daily and rats were sacrificed on the 16th day. The ovaries, adrenals, liver, kidney, and uterus were removed and weighed, and the ovary from each animal was serially sectioned and stained for histologic studies. The hemicastrated control group revealed a significant increase in ovarian weight with 45% hypertrophy and a significant increase of total healthy and atretic follicles when compared with sham-operated control rats. Treatment with 2.5 and 3.5 mg methyl parathion revealed no change in the ovarian weight with 48 and 42% hypertrophy, respectively, and no change in healthy and atretic follicles when compared with hemicastrated oil-treated controls. However, treatment with 4.0 and 5.0 mg methyl parathion resulted in a significant decrease in ovarian weight gain with 13 and 8% hypertrophy, respectively, a significant decrease in the number of healthy follicles, and no change in the atretic follicles. The number of estrous cycles and duration of each estrous cycle were affected significantly with 3.5, 4.0, and 5.0 mg methyl parathion treatment when compared with controls. There were no significant changes in adrenal, liver, kidney, or uterine weight in the methyl parathion-treated groups except a decrease in uterine weight with 5.0 mg treatment when compared with oil-treated hemicastrated controls.

Animals↗
PubMedDate not supplied

Factors influencing parathion degradation by recombinant Escherichia coli with surface-expressed organophosphorus hydrolase.

A unique approach for organophosphorus pesticides detoxification was developed previously by anchoring organophosphorus hydrolase (OPH) onto the surface of Escherichia coli with a tightly regulated tac promoter. The resulting recombinant cells degraded parathion very effectively without the diffusional limitation observed in cells expressing OPH intracellularly. However, the precise conditions for surface targeting or pesticide degradation were not fully understood. In this paper, several factors influencing parathion degradation were investigated. Production of active OPH onto the cell surface was highly host-specific; a high rate of parathion degradation was observed from strains JM105 and XL1-Blue, which regulated production of the OPH fusion very tightly. However, in the absence of ampicillin selection, plasmids were only favorably maintained in strain XL1-Blue. OPH activity was highly dependent on growth conditions. Optimal OPH activity was observed when cells were grown in Luria-Bertani (LB)-buffered medium at 37 degrees C. OPH activity was further improved by supplementing the growth medium with cobalt chloride, which favors the formation of the metal active center. The timing of cobalt addition also influenced parathion degradation. Maximum OPH activity was obtained by adding cobalt to induced cultures during the late stationary phase. The resulting cultures grown under the optimized conditions had an eight-fold increase in parathion degradation.

Aryldialkylphosphatase↗
PubMed2006

NMR investigation of the behavior of an organothiophosphate pesticide, methyl parathion, sorbed on clays.

The decomposition of methyl parathion (an organothiophosphate pesticide) sorbed on partially hydrated kaolin and montmorillonite clays (in Ca2+, Cu2+, Zn2+, and Al3+ forms) at high concentration (typically 1-10 wt %) has been examined by nuclear magnetic resonance (NMR), using solid-state 31P NMR (based on magic-angle spinning and cross polarization or direct polarization) and liquid-state 31P NMR of DMSO and acetone extracts. The results indicate that methyl parathion is initially physisorbed, appearing by solid-state 31P NMR to exhibit substantial molecular-level motion. The signals due to unreacted methyl parathion diminish and are replaced by new 31P NMR peaks resulting from hydrolysis, isomerization, and oxidation reactions over periods ranging from hours to years. 31P NMR characteristics indicate that these decomposition products are much more tightly bound to the clay than is methyl parathion. Methyl parathion decomposition is most effectively catalyzed by partially hydrated Cu(II)- and Al-montmorillonites (but with different product distributions); Ca-montmorillonite and kaolin were least effective.

Adsorption↗
PubMed2000

Paraoxon and parathion hydrolysis by aqueous molybdenocene dichloride (Cp2MoCl2): first reported pesticide hydrolysis by an organometallic complex.

We report the first case of an organometallic complex that effectively hydrolyzes the organophosphate pesticides parathion and paraoxon. The complex is the water-soluble compound bis(eta 5-cyclopentadienyl)molybdenum(IV) dichloride (1), which hydrolyzes parathion to produce ethanol and deethyl parathion in a biphasic reaction in D2O. Rate accelerations were 130 and 10(5) at pH 7 and 3, respectively. Paraoxon is readily hydrolyzed by 1 to yield p-nitrophenol and diethyl phosphate with rate accelerations of 2300 and 27 at pH 7 and 3, respectively. Kinetic data for paraoxon hydrolysis by 1 are consistent with a process that involves intermolecular (delta S++ = -49 +/- 10 eu) hydroxide attack on the phosphate triester in which the aquated 1 serves as a coordinated Lewis acid that activates the organophosphate. Interestingly parathion hydrolysis by 1 occurs via nucleophilic attack at the alpha-carbon of the phosphorothioate pesticide that involves C-O bond cleavage. These parathion results represent one of the few cases of this type of unusual hydrolytic chemistry and the first case of an organometallic complex that accelerates organophosphate pesticide hydrolysis.

Catalysis↗
PubMedDate not supplied

Effect of phenobarbitol pretreatment on regeneration of plasma cholinesterase activity inhibited by parathion or dichlorovos.

Rats were pretreated with phenobarbitol [PB (75 mg/kg, IP)] for 3 days and subsequently injected with parathion, an organophosphorous insecticide, which requires microsomal activation for its anticholinesterase effect or with dichlorovos, a cholinesterase (ChE) inhibitor as such. The difference in the mortality and spontaneous regeneration of inhibited plasma ChE by IP administration of the two insecticides was compared. A single dose of 10 mg/kg parathion caused 100% mortality in PB-untreated rats, but effected no mortality in PB-pretreated rats. A lower dose (7.5 mg/kg) of parathion resulted in plasma ChE levels which were 5, 5, 17, and 93% of initial values in PB-untreated rats and 85, 97, and 92% of initial values in PB-pretreated rats at 2-hr, 1-3-, and 5-day periods, respectively. Mortality resulting from single dose of 30 mg/kg dichlorovos was 30% in PB-pretreated, as well as untreated rats. A lower dose of dichlorovs (20 mg/kg) resulted in plasma ChE activity which was 48, 82, 90, and 97% of initial levels in PB-untreated rats, and 60, 100, 100, and 130% in PB-pretreated rats at 2 hr, 1, 3, and 5 day's, respectively. Administration of 2 mg/kg parathion for 3 days did not affect cytochrome P-450 levels in liver microsomes, but administration of 6 mg/kg dichlorovos for 3 days caused greatly lowered levels of liver microsomal cytochrome P-450, resulting from its inactivation to cytochrome P-420. Phenobarbital caused accelerated in vitro ChE regeneration in the case of dichlorovos-inhibited enzyme in the plasma, but not in the case of parathion-inhibited enzyme.

Animals↗