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PubMed1997

Temporal effect of methyl parathion on ovarian compensatory hypertrophy, follicular dynamics and estrous cycle in hemicastrated albino rats.

Methyl parathion, an organophosphorus pesticide, was administered i.p. at a dose of 5 mg/kg body weight to hemicastrated virgin rats for 1, 5, 10 and 15 days. Treatment with methyl parathion for 1 and 5 days revealed no change in the ovarian weight with -0.64% and -9.63% hypertrophy respectively and no change in healthy and atretic follicles when compared with hemicastrated oil-treated controls. However, treatment with methyl parathion for 10 and 15 days resulted in a significant decrease in ovarian weight gain with -21.36% and -31.98% hypertrophy, respectively, a significant decrease in the number of healthy follicles, and no change in the number of atretic follicles. The number of estrous cycles and duration of each phase of the estrous cycle were significantly affected with methyl parathion treatment for 5, 10 and 15 days. However, there were no significant changes in the number of estrous cycles and duration of estrus and metestrus phases in 1 day methyl parathion treatment except for a decrease and increase in proestrus and diestrus phases respectively. The weight of the uterus was significantly decreased whereas those of the liver, kidney and adrenal did not change in any of the methyl parathion treated groups.

Animals↗
PubMed2001

Effects of parathion on acetylcholinesterase, butyrylcholinesterase, and carboxylesterase in three-spined stickleback (Gasterosteus aculeatus) following short-term exposure.

The sensitivity of butyrylcholinesterase (BChE) toward the inhibition by the organophosphorus insecticide (OP) parathion-ethyl was compared with that of other esterases in the fish three-spined stickleback. Earlier field and in vitro results had suggested the higher sensitivity to OPs of stickleback BChE when compared with acetylcholinesterase (AChE). In the present study, stickleback were exposed in vivo under environmentally realistic conditions using a short duration of exposure (1 h) and parathion concentrations of 0.01, 0.1, and 1.0 microgram/L. Seventy and 80% of nominal concentrations, respectively, were measured in the 0.01 and 0.1 microgram/L treatments. Following exposure, stickleback were maintained in clean water for 48 h (recovery), allowing the metabolic activation of parathion. After recovery, the activities of BChE (axial muscle, gills, liver), AChE (brain, axial muscle, gills), and carboxylesterase (CaE, liver) were determined. Following exposure to 1 microgram/L parathion, the BChE activity was significantly decreased in liver (approximately 60%) and axial muscle (approximately 30%), while its decrease in gills (approximately 30%) was not significant. No effects on BChE activity were observed with 0.1 and 0.01 microgram/L parathion. The AChE and CaE activities remained unaffected with all parathion concentrations used. The results are discussed with respect to the potential application of stickleback BChE as a biomarker of OP exposure.

Acetylcholinesterase↗
PubMed1991

Poisoning of Canada geese in Texas by parathion sprayed for control of Russian wheat aphid.

Approximately 200 Canada geese (Branta canadensis) died at a playa lake in the Texas Panhandle shortly after a winter wheat field in the basin adjacent to the lake was treated with parathion to control newly invading Russian wheat aphids (Diuraphis noxia). No evidence of infectious disease was diagnosed during necropsies of geese. Brain ChE activities were depressed up to 77% below normal. Parathion residues in GI tract contents of geese ranged from 4 to 34 ppm. Based on this evidence, parathion was responsible for the goose mortalities. Parathion applications to winter wheat will undoubtedly increase if parathion is applied for control of both Russian wheat aphids and greenbugs (Schizaphis graminum). Geese may potentially be exposed to widespread applications of parathion from fall to spring, essentially their entire wintering period.

Aerosols↗
PubMed1999

Effect of methyl parathion formulation on estrous cycle and reproductive performance in albino rats.

The animals were injected intraperitoneally with graded doses of methyl parathion at 1.5 to 3 mg/kg body weight for 15 days from the day of estrus. Results indicated that the methyl parathion treatment showed irregular estrous cycles, affect the duration of each estrous cycle, proestrus and diestrus were significantly changed in 2.5 and 3 mg treatment groups. But there was no significant change in the number and duration of each estrous cycle, duration of proestrus and diestrus in 1.5 and 2 mg methyl parathion treatment groups. However, there was a significant decrease in the duration of estrus, while there was no significant change in the duration of metestrus in all methyl parathion treatment rats when compared with those of the corresponding parameters of the control. There was no significant effect on number of live pups on day 1 and 5 except in 3 mg methyl parathion treatment group where it was significantly decreased. There was no significant change in reproductive indices like pregnancy, parturition, live birth and viability in all the methyl parathion treatment rats except the viability index in the highest dose.

Animals↗
PubMed2005

Degradation of parathion and the reduction of acute toxicity in TiO2 photocatalysis.

Photocatalytic degradation of methyl parathion was done using a circulating TiO2/UV and TiO2/solar reactor. Indoor experimental results showed that, under the photocatalysis conditions, parathion was more effectively degraded than under the photolysis and TiO2 only conditions. Parathion (38 microM) was completely degraded under photocatalysis within 90 min, and more than 80% TOC decrease after 150 minutes. The main ionic byproducts during the photocatalysis were measured, and almost complete nitrogen recovery was achieved as mainly NO3- NO2-, and NH4+, and 80% of sulfur as recovered as SO4(2)-. Organic intermediates such as nitrophenol and methyl paraoxon were also identified during the photocatalysis of parathion, and these were further degraded after 90 minutes. Microtox bioassay using Vibrio fischeri was used in evaluating the toxicity of solutions treated by photocatalysis and photolysis of parathion. The results showed that the acute toxicity expressed as EC50 almost reduced after 90 min under the photocatalysis condition whereas only 40% reduction of toxicity as EC50 was achieved in photolysis condition. The outdoor results using a TiO2/solar system were similar to the TiO2 indoor system, indicating the possibility of applying TiO2/solar system for the treatment of parathion-contaminated water.

Biological Assay↗
PubMedDate not supplied

Methyl parathion acute toxicity: prophylaxis and therapy with memantine and atropine.

Male rats administered with a single i.p. dose of 5 mg/kg methyl parathion, showed the toxic signs of hypercholinergic (anticholinesterase) activity with maximal severity, including muscle fasciculations and convulsions within 15 to 30 min, persisting for about 2 hr. The time course of acetylcholinesterase activity in discrete brain regions (cortex, stem, striatum and hippocampus), heart and hemidiaphragm, indicated its maximal depression during 30 to 60 min after administration of methyl parathion. At this time, a marked reduction in carboxylesterase activity was also evident both in neuronal and nonneuronal tissues, suggesting a tremendous binding to nonacetylcholinesterase serine sites. Pretreatment with memantine hydrochloride (18 mg/kg, i.p.) 30 min, and atropine sulfate (16 mg/kg, i.p.) 15 min before methyl parathion administration, completely prevented the expected toxic signs and significantly (P less than 0.01) attenuated the induced inhibition of acetylcholinesterase. When given therapeutically, this combined treatment completely reversed the clinical evidence of methyl parathion toxicity within 10 to 15 min and markedly reduced the acetylcholinesterase inactivation. These results suggest that memantine may counteract the acute methyl parathion toxicity by (a) protection of acetylcholinesterase from inhibition, (b) rapid reactivation of inhibited acetylcholinesterase and (c) rapid bioelimination of methyl parathion, in addition to cholinolytic effects of atropine sulfate.

Acetylcholinesterase↗
PubMed1983

Colorimetric method for field-screening above-tolerance parathion residues on and in citrus fruits.

A colorimetric technique has been developed which is suitable for use as a field-screening method for detecting above-tolerance levels of parathion on and in citrus fruits. By using this method, a grower should be able to postpone harvesting a crop until parathion residues are below tolerance level, so that the crop is safe to market. The method depends on the reaction of parathion with 4-(p-nitrobenzyl)-pyridine. Parathion is extracted by mixing chopped citrus rind with acetone in a hand-operated homogenizer. The extract is partially cleaned by a partitioning step before final cleanup with a Sep-Pak Florisil cartridge. The colored reaction solution is read at 560 nm by using a portable, rechargeable spectrophotometer. A single test can be completed in about 75 min; the average time per test when several are conducted sequentially is considerably shorter. The analytical system responds readily to less than 5 ppm parathion on or in 1 g navel orange rind, which corresponds to less than 1 ppm in the whole fruit. The present U.S. tolerance for parathion on or in citrus is 1 ppm on a whole fruit basis. Preliminary work indicates that the method should also be suitable for apples.

Citrus↗
PubMedDate not supplied

Association between indoor residential contamination with methyl parathion and urinary para-nitrophenol.

Methyl parathion, a pesticide listed by the U.S. Environmental Protection Agency in Toxicity Category I (i.e., most toxic), is not licensed for indoor use, and human exposure has resulted in the deaths of infants and children. From January 1991 through November 1994, an unlicensed pesticide applicator sprayed the interior of more than 200 homes in Lorain County, Ohio, with methyl parathion. To measure the environmental contamination this spraying caused, we measured methyl parathion in residential samples (air filtration and surface wipe) collected from a subset of 64 homes. To measure human exposure, we collected urine samples from 142 people living in these homes and measured urinary levels of para-nitrophenol, a methyl parathion metabolite. We then used a generalized estimating equation to evaluate the association between residential contamination and human exposure. The model included the age of the resident, the number of days between pesticide application and sample collection, and air and surface-wipe methyl parathion concentrations. As expected, the air and surface-wipe concentrations each had a significant inverse relationship with the number of days between application and sample collection. The model explained 65.7% of the variation in urinary para-nitrophenol concentrations. The form of this model could be used to estimate urine p-nitrophenol in residents exposed to methyl parathion in situations where urine specimens are not available. We recommend site-specific validation of this model.

Adolescent↗
PubMed1997

Comparative evaluation on the biological monitoring of exposure to parathion and its methyl analog.

The effects of both parathion and methyl parathion on the inhibition of plasma cholinesterase were elaborated in a rat model employing a modified isocratic reverse-phase HPLC method coupled with UV detection for the determination of the urinary metabolite p-nitrophenol (U-4NP). A linearity of r2 > 0.995 was found for a standard curve ranging from 0.06 to 0.96 microg/mL with a % relative error of </= +/- 10% and a recovery of 89 +/- 2%. The % CV at all levels was </= 11%. A linear correlation was observed between the oral administration of parathion and methyl parathion for both the percent inhibiton of cholinesterase as well as the urinary elimination of 4NP. It is tentatively recommended that an U-4NP of 2. 0 mg/g creatinine be established as a biological exposure index (BEI) for methyl parathion.

Animals↗
PubMed1992

Comparative metabolism of methyl parathion in intact and subcellular fractions of isolated rat hepatocytes.

Metabolism of the widely used insecticide methyl parathion by isolated hepatocytes and various subcellular fractions was compared to determine the effects of cellular integrity on the metabolic profile observed. A reverse-phase ion-pair high-performance liquid chromatographic method was developed to separate and quantify methyl parathion and six of its hepatic biotransformation products: methyl paraoxon; desmethyl parathion; desmethyl paraoxon; p-nitrophenol; p-nitrophenyl glucuronide; and p-nitrophenyl sulfate. Most compounds exhibited linear responses and limits of detection below 1 nmol. The chromatographic method was used to determine metabolic profiles of methyl parathion in isolated rat hepatocytes, sonicated hepatocytes, postmitochondrial fraction, microsomes, and cytosol. Isolated hepatocytes produced significantly more desmethyl parathion and p-nitrophenyl sulfate than the subcellular preparations, demonstrating that cellular integrity significantly affects the quantitative metabolic profile observed.

Animals↗
PubMed2001

Changes induced by malathion, methylparathion and parathion on membrane lipid physicochemical properties correlate with their toxicity.

Perturbations induced by malathion, methylparathion and parathion on the physicochemical properties of dipalmitoylphosphatidylcholine (DPPC) were studied by fluorescence anisotropy of DPH and DPH-PA and by differential scanning calorimetry (DSC). Methylparathion and parathion (50 microM) increased the fluorescence anisotropy evaluated by DPH-PA and DPH, either in gel or in the fluid phase of DPPC bilayers, but mainly in the fluid phase. Parathion is more effective than methylparathion. On the other hand, malathion had almost no effect. All the three xenobiotics displaced the phase transition midpoint to lower temperature values and broadened the phase transition profile of DPPC, the effectiveness following the sequence: parathion>methylparathion>>malathion. A shifting and broadening of the phase transition was also observed by DSC. Furthermore, at methylparathion/lipid molar ratio of 1/2 and at parathion/lipid molar ratio of 1/7, the DSC thermograms displayed a shoulder in the main peak, in the low temperature side, suggesting coexistence of phases. For higher ratios, the phase transition profile becomes sharp as the control transition, but the midpoint is shifted to the previous shoulder position. Conversely to methylparathion and parathion, malathion did not promote phase separation. The overall data from fluorescence anisotropy and calorimetry indicate that the degree of effect of the insecticides on the physicochemical membrane properties correlates with toxicity to mammals. Therefore, the in vivo effects of organophosphorus compounds may be in part related with their ability to perturb the phospholipid bilayer structure, whose integrity is essential for normal cell function.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1984

Genotoxicity of methyl parathion in short-term bacterial test systems.

Genotoxicity of the insecticide methyl parathion was investigated in Salmonella typhimurium and Escherichia coli bacterial test systems for the detection of back mutations and DNA-damage. Methyl parathion was mutagenic to S. typhimurium strain TA100 after activation with rat liver microsomal and cytosolic enzymes. In DNA repair tests, methyl parathion was effective in inducing damage to the S. typhimurium strain TA1538 which lack excision repair compared to the strain TA1978 which is proficient in excision repair mechanisms. Normal laboratory light conditions had no effect on the mutagenicity tests, however, exposure of methyl parathion in the petri dish containing the tester strain TA100 and rat liver microsomal and cytosolic enzymes reduced the mutagenic activity and increased the toxic effects of methyl parathion.

DNA Repair↗
PubMed1989

Effects of subchronic parathion administration on sodium salicylate excretion kinetics in female rats.

Organophosphorus (OP) pesticides are considered to be environmental contaminants, and chronic exposure to low levels through the diet may affect drug action. To study this possible interaction, ethyl parathion was administered by intubation to female rats for 35 consecutive days at a dose of 0.05 or 0.2 mg/kg of body weight per day. At 7, 21 and 35 days after parathion was initiated, rats were administered a single dose of 20 mg/kg sodium salicylate intraperitoneally. Total salicylates, salicylic acid (SA), salicyluric acid (SU) and gentisic acid (GA) were determined in urine. At 7 days, parathion treatment slowed the excretion of total salicylates. This effect was more evident at longer treatment times. Total excretion of SA was increased at the expense of GA at 7 days. However, this effect was reversed at 21 and 35 days. Excretion of SU was drastically diminished after 21 days of treatment with parathion. The results suggest that subchronic oral administration of parathion to female rats changes the excretion kinetics of sodium salicylate through combined effects on renal excretion mechanisms and biotransformation processes. Thus, exposure to low concentrations of environmental contaminants may produce important changes in drug action.

Animals↗
PubMed2001

Biochemical factors contributing to response variation among resistant and sensitive clones of Daphnia magna Ssraus exposed to ethyl parathion.

Biochemical factors contributing to response variation in five clones of Daphnia magna exposed to ethyl parathion were studied. Differences in sensitivities to ethyl parathion between sensitive and resistant clones varied between four- and ninefold. Acute toxicity and in vivo acetylcholinesterase (AChE) inhibition responses to ethyl parathion were similar, whereas in vitro AChE sensitivities to paraoxon were higher. Thus indicating that, in vivo, not all ethyl parathion present is converted by Daphnia juveniles to active metabolite, or if so, only a proportion of the paraoxon produced is in direct contact with its target. Comparison of AChE activities obtained during in vitro and in vivo exposures with acute responses revealed clonal concordance only between in vivo AChE sensitivities and acute toxicity. This latter finding indicates that clonal differences in ethyl parathion metabolism rather than differences in AChE sensitivities are the most likely explanations of the observed genetic differences in tolerance.

Animals↗
PubMed1998

Learning and memory of rats after long-term administration of low doses of parathion.

A set of four learning and memory tests (Morris Maze I for reference memory, Morris Maze II for working memory, one-way active avoidance, and passive avoidance) were employed to address the questions whether parathion impaired cognitive functions after low, long-term exposure and could cause persistent changes in cognition. Motor activity and general behavior were investigated in a functional observational battery. Parathion was administered in rat food in low doses which caused no clinical symptoms and no or borderline brain acetylcholinesterase inhibition. Parathion doses of 0.5, 2, or 8 ppm in rat food produced the averaged uptake of 24, 100, or 400 microg/kg body weight per group per day in male rats and 36, 152, or 550 microg/kg per day in female rats in week 13. Learning tests were performed in weeks 1 to 4 and 10 to 14, as well as 30 to 34 weeks after the end of treatment, when the male and female rats were about 13 months old. Low doses of parathion given daily for 13 weeks had no cumulative or adverse effects on learning and memory, either during treatment or after the extended treatment-free period, in any of the tests. A significant improvement of learning compared to control observed in the Morris Water Maze I during the first week of treatment (males dose group 0.5 ppm) shows that parathion can improved cognitive functions in rats. Results of the study indicate that adverse effects changing learning and memory in animals may occur only at higher doses of organophosphates, at which the peripheral and brain acetylcholinesterases are inhibited to a greater extent than those in the present study.

Animals↗
PubMed1992

Chronic toxicity of ethyl parathion and isobutoxyethanol ester of 2,4-dichlorophenoxyacetic acid to estuarine juvenile and adult crabs.

The chronic toxicity of ethyl parathion and isobutoxyethanol ester of 2,4-dichlorophenoxyacetic acid was determined for the crabs Uca uruguayensis and Chasmagnathus granulata collected in Argentina in 1989. Parathion toxicity was more time-dependent than 2,4-D. Four-week LC50 values for parathion were size and species independent, as expected under chronic exposure conditions. As shown in previous studies, the opposite was noted when crabs were exposed to acute exposure. Parathion was much more toxic than 2,4-D, in all cases. Also, parathion exerted a very much lower chronic lethal effect than other pesticides at a fraction of the respective acute LC50. A different susceptibility between sexes was found in C. granulata exposed to 2,4-D.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1978

Binding of the organophosphates parathion and paraoxon to bovine and human serum albumin.

Binding of parathion and paraoxon to bovine serum albumin (BSA) and human serum albumin (HSA) was studied by using equilibrium dialysis. The concentration of unbound organophosphate was determined from its anticholinesterase activity. Binding of parathion to BSA was shown to be reversible. The organophosphates interact with only one type of binding sites in BSA and HSA. The affinity constants at pH 7.2 and 4 degrees C for the interaction of BSA or HSA and parathion were found to be 2.7 X 10(6) and 1.5 X 10(6) M-1, respectively. The affinity constants for the interaction of the serum albumins and paraoxon were considerably lower, 6.0 X 10(3) and 1.6 X 10(4) M-1, respectively. Lowering the pH from 7.2 to 4.8 did not significantly affect the binding parameters. The great difference of affinity of the serum albumins to parathion and paraoxon is discussed with respect to the fate of parathion in the body.

Animals↗
PubMed1983

Parathion alters incubation behavior of laughing gulls.

One member of each pair of incubating laughing gulls at 9 nests was trapped, orally dosed with either 6 mg/kg parathion in corn oil or corn oil alone, and marked about the neck with red dye. Each nest was marked with a numbered stake and the treatment was recorded. A pilot study with captive laughing gulls had determined the proper dosage of parathion that would significantly inhibit their brain AChE activity (about 50% of normal) without overt signs of poisoning. After dosing, birds were released and the nests were observed for 2 1/2 days from a blind on the nesting island. The activities of the birds at each marked nest were recorded at 10-minute intervals. Results indicated that on the day of treatment there was no difference (P greater than 0.05, Chi-square test) in the proportion of time spent on the nest between treated and control birds. However, birds dosed with 6 mg/kg parathion spent significantly less time incubating on days 2 and 3 than did birds receiving only corn oil. By noon on the third day, sharing of nest duties between pair members in the treated group had approached normal, indicating recovery from parathion intoxication. These findings suggest that sublethal exposure of nesting birds to an organophosphate (OP) insecticide, such as parathion, may result in decreased nest attentiveness, thereby making the clutch more susceptible to predation or egg failure. Behavioral changes caused by sublethal OP exposure could be especially detrimental in avian species where only one pair member incubates or where both members are exposed in species sharing nest duties.

Animals↗