• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.17 no.4
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• pp.300-309
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• 2007

Although parathion is an organophosphate pesticide being legally applied for the purpose of agriculture and is being manufactured, parathion in the air and urinary p-nitrophenol, a metabolite of parathion, were not analysed in Korea. Air of the parathion manufacturing workplace was sampled by OVS-2 tubes using NIOSH 5600 and spot urine of workers was sampled at the end of shift. Parathion and urinary p-nitrophenol were analysed by GC/MS (5973 MSD connected with Agilent 6890 GC) and the protocol was included in this study. It was found that this protocol should be so sensitive that determining parathion in the air and urinary p-nitrophenol below level of ACGIH TLV and BEI be adequate. Another finding was that total sampling volume of air of NIOSH 5600 of 240 L should be adjusted to be less than 120 L due to breakthrough.

• Korean Journal of Veterinary Service
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• v.15 no.1
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• pp.58-66
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• 1992

The insecticide p-nitropheny diethyl thiophospate is alse known by the symbol E.605 and a legion of trade names including “parathion”. The insecticide is widely used in agriculture, but it is highly toxic and now clear that parathion behaves like a cholinergic drug by inhibiting the enzyme cholinesterase. In order to know acute toxicity and the changes of glucose concentrations and activity according to time lapsed in female mice given orally single with the half dose to $LD_{50}$ of parathion, glucose contents and cholinesterase activities in serum as well as cholinesterase activities in whole brain and spinal cord were investigated, otherwise median lethal dose ($LD_{50}$) of parathion given orally against female mice was determined. The results obtained were summerized as follows ; 1. $LD_{50}$ value of parathion given orally to female mice was 7.1mg/kg(95% confidence limits, 3.8-13.1mg/kg) 2. The inhibition rate of cholinesterase activities in serum of parathion-administrated mice according to time lapsed were peakly decreased to 61% after 30 minutes in comparison to control group, but activities were completely recovered after 48 hours. 3. The inhibition rate of cholinesterase activities in whole brain of parathion-administrated mice according to time lapsed were peakly decreased to 49% after 2 hours in completely recovered after 24 hours. 4. The inhibition rate of cholinesterase activities in spinal cord of parathion-administrated mice according to time lapsed were peakly decreased to 57% after 2 hours in comparison to control group, but activities were completely recovered after 48 hours. 5. The changes of glucose contents in serum of parathion-administrated mice according to time lapsed and in directly after death due to parathion poisoning were no significantly difference.

• Archives of Pharmacal Research
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• v.14 no.4
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• pp.330-335
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• 1991

The effects of physostigmine and neostigmine on the parathin induced toxicity were examined in adult female rats. Physostigmine $(100\;{\mu}g/kg,\;ip)$ or neostigmine $(200\;{\mu}g/kg,\;ip)$ inhibited acetylcholinesterase (AChE) and cholinesterase (ChE) activities in blood, brain and lung when the enzyme activity was measured 30 min after the treatment. At the doses of two carbamates equipotent on brain AChE, neostigmine showed greater inhibition on peripheral AChE/ChE. The enzyme activity returned to normal in 120 min following the carbamates except in the lung of rats treated with neostigmine. Carbamates administered 30 min prior to parathion (2 mg/kg) antagonized the inhibition of AChE/ChE by parathion when the enzyme activity was measured 2 hr following parathion. Neostigmine showed greater protective effect on peripheral AChE/ChE. The effect of either carbamate on AChE/ChE was not significant 2 hr beyond the parathion treatment. Carbamates decreased the mortality of rats challenged with a lethal dose of parathion (4 mg/kg, ip) either when treated alone or in combination with atropine (10 mg/kg, ip). Lethal action of paraoxon (1.5 mg/ks ip), the active metabolite of parathion was also decreased by the carbamate treatment indicating that the protection was not mediated by competitive inhibition of metabolic conversion of parathion to paraoxon. The results suggest that carbamylation of the active sites may not be the sole underlying mechanism of protection provided by the carbamates.

• Journal of Korean Society of Environmental Engineers
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• v.27 no.8
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• pp.822-828
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• 2005

The photocatalytic degradation of methyl parathion was carried out using a circulating $TiO_2$/solar system. Under the photocatalytic condition, parathion was more effectively degraded than by the photolysis or $TiO_2$ only condition. The parathion degradation followed pseudo first-order kinetics. With photocatalysis, 10 mg/L parathion was completely degraded within 90 min with a TOC decrease exceeding 63% after 150 min. The nitrogen from parathion was recovered mainly as ${NO_2}^-$, ${NO_3}^-$, and ${NH_4}^+$, 80% of sulfur as ${SO_4}^{2-}$, and less than 5% of phosphorus as ${PO_4}^{3-}$ during photocatalysis. The organic intermediates 4-nitrophenol and paraoxon were also identified, and these were further degraded. Two different bioassays using V. fischeri and D. magna were employed to measure the toxicity reduction in the solutions treated by both photocatalysis and photolysis. Relative toxicity was reduced almost completely after 150 min in both organisms under the photocatalysis, whereas in photolysis, 76 and 57% reduction was achieved for V. fischeri and D. magna, respectively. The acute toxicity reduction pattern corresponded with the decrease in parathion and TOC concentrations.

• Toxicological Research
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• v.6 no.1
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• pp.51-59
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• 1990

Effects of altering hepatic mixed-function oxidase (MFO) enzyme activities on the metabolism and acute toxicity of parathio were investigated in adult female rats. In vitro hepatic metabolism of parathion to paraoxon was increased by phenobarbital pretreatment (50 mg/kg/day, ip, for 4 consecutive days) and SKF 525-A (50 mg/kg, ip, 1 hr prior to sacrifice) decreased paraoxon formation indicating that phenobarbital induces that form(s) of cytochrome P-450 catalyzing conversion of parathion to paraoxon. Degradation of paraoxon to p-nitrophenol was increased by phenobarbital pretreatment, but not affected by SKF 525-A suggesting that MFO activities play only a minor role in the detoxification of the active metabolite of this insecticide. The phenobarbital-induced increase in paraoxon formation was partially antagonized by SKF 525-A. Significant activity for both parathion activation and paraoxon degradation was also observed in the lung preparation, however, this extrahepatic parathion and paraoxon metabolizing activity was not induced by phenobarbital or inhibited by SKF 525-A pretreatment. Phenobarbital pretreatment increased paraoxon level in livers of rats when measured 3 hr following parathion injection (2 mg/kg, ip). SKF 525-A did not alter parathion or paraoxon levels in brain, blood and liver. Phenobarbital pretreatment decreased the toxicity of parathion (4mg/kg, ip) or paraoxon (1.5 mg/kg, ip) as determined by decreases in lethality and inhibition of brain and lung acetylcholinesterases. An additional SKF 525-A treatment failed to decrease the protective effects of phenobarbital against parathion or paraoxon toxicity. These results suggest that some unknown factors other than hepatic MFO induction are involved in the protective action of phenobarbital against parathion and paraoxon toxicity.

• Journal of Environmental Health Sciences
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• v.30 no.3
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• pp.214-220
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• 2004

The microcosm type wetland systems were constructed in order to treat wastewater contaminated with parathion. The microcosm reactor consisted of marsh and pond type. The experiment was carried out using batch (marsh or pond) and continuous (marsh-pond and pond-marsh type) systems. In the batch reactor, marsh-type wetland completely removed parathion in water within 8 days, while pond reactor removed 97% of parathion during the same period. During parathion degradation, the amount of 4-nitrophenol production, one of the metabolites from parathion degradation, was higher in marsh-type batch reactor. In the continuous systems, both marsh-pond and pond-marsh combination systems effectively removed parathion from water, and the production of 4-nitrophenol was also minimal. In the extraction experiment, the parathion and its metabolite were not found in the wetland soil and the plant. In order to achieve both aerobic and anaerobic conditions, the continuous wetland system combining marsh and pond type can be the alternative for the non-point source pollutants such as parathion pesticide.

• Proceedings of the Korean Society of Soil and Groundwater Environment Conference
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• 1999.10a
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• pp.3-6
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• 1999

Several chemical washing procedures were applied to Parathion and Diazinon contaminated soil. Batch and column tests were performed to determine the insecticides extraction efficiency as a function of pH. Washing efficiency of methanol is more higher than that of water and HCl when washed parathion and diazinon are. Those are completely miscible with most organic solvents. For parathion, release trend is increased as pH is increased because it is hydrolyzed easily at the condition of alkali. But diazinon shows reverse because diazinon is decomposed rapidly at the condition of acidic So, diazinon is more released than parathion is because this experiment is peformed in acidic and weak acidic conditions. Generally, parathion and diazinon are classified as having low mobility, so they can be easily controlled if the proper washing process are applied.

• Bulletin of the Korean Chemical Society
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• v.29 no.5
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• pp.985-987
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• 2008

Parathion is an organophosphate pesticide being legally applied for the purpose of agriculture and is being manufactured in Korea. A gas chromatography/mass spectrometric method was developed for the determination of parathion urinary metabolite, p-nitrophenol. p-Nitrophenol was extracted from weak acidic urine, and then measured by gas chromatography-mass spectrometry (selected ion monitoring). The recovery of pnitrophenol in the overall procedure was 88.2%. The detection limit of the assay was 1.0 $\mu$ g/L based upon assayed urine of 2.0 mL. The method was applied to the determination of p-nitrophenol in urine of workers of a parathion industry. Spot urines of workers of a parathion industry were sampled at the end of shift and pnitrophenol was analyzed using above developed method. p-Nitrophenol could be detected in all of the urine samples at concentrations varying from 3.0 to 681 $\mu$ g/L.

• Korean journal of applied entomology
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• v.35 no.3
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• pp.254-259
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• 1996

The biochemical factors responsible for parathion resistance in a ethyl fenitrothion-selected Yumenoshima I11 (EF-30) strain of the housefly were examined. Great difference (167-fold) in the Iso was observed between the resistant EF-30 (R) and susceptible SRS (S) strains in vitro, suggesting that altered acetylcholinesterase (AChE) in the housefly strain was an important factor in the resistance. The in vitro degradative activity of parathion and paraoxon in both strains was associated with the microsomal and soluble fractions and required NADPH and reduced glutahione (GSH), respectively. The R strain possessed higher activity for GSH S-transferase than the S strain, and this enzyme appears to be important in the resistance mechanism. The R strain was highly resistant to parathion (101,487-fold), but substitution of the methoxy group for ethoxy group decreased the resistance level (25,914-fold) and parathion could be a substrate of GSH S-transferase. It is concluded that the combination of some factors (altered AChE, and enhanced activity of cytochrome P450 dependent monooxygenase and GSH S-transferase) could be sufficient to account for the extremely high level of resistance to parathion and parathion-methyl, although a possible involvement of other factor(s) can not be excluded.

• Korean Journal of Veterinary Service
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• v.14 no.1
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• pp.71-77
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• 1991

Parathion is widely used in agriculture, but it is highly toxic and now clear that parathion behaves like a cholinergic drug by inhibiting the enzyme cholinesterase. In order to know acute toxicity and the changes of cholinesterase activity according to time lapsed in Sprague-Dawley rats injected single with half dose to LD$_{50}$ of parathion, cholinesterase activities in serum, spinal cord, whole brain and median lethal dose between sex difference were investigated. The results obtained were summerized as follows ; 1. 4LD_{50}$ values of parathion given intraperitoneally to male and female rats were 10.5mg / kg(95% confidence limits, 6.6-16.8mg/ kg) and 3.3mg/ kg(95% confidence limits, 1.9-5.6mg/ kg). 2. The inhibition rate of cholinesterase activities in serum of parathion-injected rats according to time lapsed were peakly decreased to 35.4%(male) and 32.4%(female) after 1 hour in comparison to control group, but cholinesterase activities were completely recovered after 48 hours. 3. The inhibition rate of cholinesterase activities in spinal cord of parathion-injected rats according to time lapsed were peakly decreased to 31.1% (male) and 36.3% (female) after 30 minutes in comparison to control group, but cholinesterase activities were completely recovered after 48 hours. 4. The inhibition rate of cholinesterase activities in whole brain of parathion -injected rats according to time lapsed were peakly decreased to 32.2%(male) and 42.6%(female) after 1 hour in comparison to control group, but cholinesterase activities were completely recovered after 48 hours.s.