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PubMedDate not supplied

Effect of high-fat and high-protein diets on toxicity of parathion and dichlorvos.

Growing male rats that weighed 120 +/- 5 g were kept for 30 days on the following synthetic diets: high protein diet (HPD), 59% casein; high fat diet (HFD), 50% saturated fat; and normal diet (ND), 19% casein, 10% saturated fat, and 60% sucrose. Other essential dietary ingredients were included in all the diets. All animals were injected at the end of the 30-day period with parathion [10 mg/kg intraperitoneal (ip) injection as a single dose] or dichlorvos (30 mg/kg ip as a single dose) to compare the effect of dietary pretreatments on mortality from parathion and dichlorvos. A lower dose of parathion (7.5 mg/kg) and dichlorvos (20 mg/kg) was employed in another set of experiments to compare the spontaneous regeneration of plasma and red blood cell (RBC) cholinesterase (ChE) activity at 2 hr, 1 day, 3 days, and 5 days after administration of parathion or dichlorvos. The effect of these diets on hepatic microsomal oxidases was also determined. Results showed that diets per se did not affect initial plasma and RBC ChE activity. The HPD and HFD significantly protected against mortality from parathion but not from dichlorvos. Hepatic microsomal cytochrome P-450 and aminopyrine demethylase activity were unchanged, but aniline hydroxylase activity was increased significantly by HPD and HFD. Parathion oxidase in hepatic microsomes was significantly increased in rats fed HFD only. For the HPD, spontaneous regeneration of ChE diminished in RBCs in parathion-intoxicated rats and in plasma and RBCs of dichlorvos-intoxicated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1978

Fate of parathion in artificially fortified grape juice processed into wine.

"Semellon" grape juice fortified with a high level of 25 ppm parathion was fermented using Saccharomyces cerevisiae var. ellipsoideus. After 12 days inte parathion levels in the wine and lees were 10.3 and 156 ppm, respectively; the paraoxon, aminoparathion, and p-nitrophenol levels in the wine were 0.16, 0.20, and 4.5 ppm, respectively, and in the lees were 0.04, 3.1 and 10 ppm, respectively. Thus, hydrolysis of parathion to p-nitrophenol and parathion sorption to sedimented particulate matter were important pathways for parathion residue reduction in the wine. The 56-day-old finished wine just prior to bottling contained 8.8 ppm parathion, 0.04 ppm paraoxon, 0.21 ppm aminoparathion, and 3.0 ppm p-nitrophenol. Two months storage at 24 degrees, 12 degrees, 4 degrees, and -20 degrees C had no effect on paraoxon and aminoparathion residue levels in the wine; parathion residues in wine decreased at all storage temperatures.

Drug Stability↗
PubMed1976

Deldrin and parathion interaction in the prostate and liver of the mouse.

The oral administration of dieldrin (1.25 mg/kg daily x 5 or 10) and/or parathion (5.2, 2.6, or 1.3 mg/kg daily x 5 or u0) caused significant alterations in the metabolism of [1,2-3H]testosterone by the anterior prostate gland and by the hepatic microsomal enzyme system in the mouse. A 5-day parathion treatment followed by another 5-day treatment with dieldrin led to significant increases in the levels of [3H]androstanediol a [3H]androstenedione formed by the prostate gland in vitro. Dieldrin alone, dieldrin plus parathion, or dieldrin administration followed by parathion treatment caused significant reductions in the levels of [3H]androstenedione formed by hepatic microsomal enzymes. Concomitantly, significant increases were observed in hepatic 7alpha-and 6beta-testosterone hydroxylase activities in animals treated with parathion followed by dieldrin administration. The present findings revealed that the administration of parathion or dieldrin leads to changes in the metabolism of male sex hormones in mouse liver and sex accessory organs. In addition, the simultaneous administration of parathion and dieldrin leads to an interaction that can alter the biologic effects of either compound.

Androgens↗
PubMed1994

Disposition of parathion after dermal application in pigs.

Pharmacokinetic parameters of parathion were studied in pigs after intravenous (i.v.) and dermal administration of unlabelled and 14C-parathion. Plasma concentration-time data were subjected to non-compartmental analysis. Intravenous injection studies showed a mean residence time (MRT) of 2.15 h, a body clearance (ClB) of 4.4 l/kg/h and a volume of distribution (Vss) of 9.8 l/kg. Dermal application led to a mean absorption time (MAT) of 78 h, and a bioavailability of 9.9%. Plasma levels of 14C-parathion (parathion + metabolites) were much higher and more persistent than those of parathion itself. After i.v. administration, recovery of 14C-parathion from urine plus faeces was almost 100% within 3 d, while it was less than 20% after dermal application. Ten days after dermal application high 14C concentrations remained in the back skin, i.e. the application area. In skin samples from areas where contamination from the application area could not have occurred, the 14C-parathion concentration was as low as 2 micrograms/g. It is concluded that in view of the low dermal bioavailability for organophosphorus insecticides it is unlikely that pour-on preparations containing these insecticides reach the ectoparasites through absorption and systemic distribution, but rather that this happens after spreading on the surface of the skin.

Absorption↗
PubMed1977

Parathion utilization by bacterial symbionts in a chemostat.

A continuous-culture device was used to select and enrich for microorganisms, from sewage and agricultural runoff, that were capable of using the organophosphorus insecticide parathion as a sole growth substrate. Parathion was dissimilated by the highly acclimated symbiotic activities of Pseudomonas stutzeri, which non-oxidatively and cometabolically hydrolyzed the parathion to ionic diethyl thiophosphate and p-nitrophenol, and P. aeruginosa, which utilized the p-nitrophenol as a sole carbon and energy source. Ionic diethyl thiophosphate was found to be inert to any transformations. Methyl parathion was dissimilated in an analogous way. The device functioned as a chemostat with parathion as the growth-limiting nutrient, and extraordinarily high dissimilation rates were attained for parathion (8 g/liter per day) and for p-nitrophenol (7 g/liter per day). This is the first report of parathion utilization by a defined microbial culture and by symbiotic microbial attack and of dissimilation of an organophosphorus pesticide in a chemostat.

Hydrolysis↗
PubMedDate not supplied

Modeling of sorption and biodegradation of parathion and its metabolite paraoxon in soil.

To investigate the distribution of parathion [O,O-diethyl O-(4-nitrophenyl) phosphorothioate] and its highly toxic metabolite paraoxon [O,O-diethyl O-(4-nitrophenyl)phosphate] between the soluble and sorbed pools in the soil, batch experiments were conducted to evaluate the rate of adsorption and desorption of 14C-labeled parathion and paraoxon in soil. The mineralization and degradation of these products were also investigated during a 56-d experiment under controlled laboratory conditions. Adsorption patterns indicated initial fast adsorption reactions occurring within 4 h for both parathion and paraoxon. We also observed the formation of nonextractable residues. The paraoxon was more intensively degraded than the parathion, and production of p-nitrophenol and other metabolites was observed. A kinetic model was developed to describe the sorption and biodegradation rates of parathion, taking into account the production, retention, and biodegradation of paraoxon, the main metabolite of parathion. After fitting the parameters of the model we made a simulation of the kinetics of the appearance and disappearance of paraoxon. From the simulation we predicted a quantity of metabolite in the liquid phase amounting to 1% of the quantity of parathion initially applied. This is in agreement with the experimental data.

Adsorption↗
PubMed1999

[Diagnosis of acute parathion intoxication and medical-legal consequences].

During a toxicological screening of a 16-year-old girl, in a clinical toxicological case, a parathion-intoxication has been detected. GC/MS revealed the presence of ethyl parathion in the gastric content and p-nitrophenol in urine. p-Nitrophenol is a major metabolite of ethyl-parathion. A serum concentration of 0.07 mg/L of ethyl parathion was measured by GC/MS-SIM. During hospitalisation the severity of parathion intoxication was monitored by measurement of pseudo-cholines-terase activities in serum. The young girl recovered well of her intoxication after a few days, without any apparent sequellae. A preliminary inquiry revealed that the adolescent had consumed a bowl of soup at the home of a 67-year-old female neighbour, who died the same day. Her corpse was found at her home. The certificate of death, written by the doctor in charge, attested a heart failure. Due to the results of the toxicological analyses from the kid, the juridical authorities ordered an autopsy of the corpse of the lady. Ethyl parathion was found in the gastric content and p-nitrophenol in urine. Even after several temptations it has not been possible to detect ethyl parathion neither in blood nor in some organs. But it was possible to detect traces of p-nitrophenol her blood.

Acute Disease↗
PubMed1975

Degradation of parathion applied to peach leaves.

Parathion was applied to peach trees in three different formulations 70 days before harvest. Leaf samples were taken periodically through the 70-day period and gas-liquid chromatographic analyses were conducted for dislodgable and penetrated residues. Analyses were also conducted for paraoxon and the s-ethyl isomer of parathion. Punched samples were compared to whole-leaf samples; generally residue levels for both types corresponded closely. A new experimental formulation, encapsulated parathion, produced highest levels of total parathion throughout the 70-day study, but even this formulation resulted in low total residue levels around 1 ppm at time of harvest. Degradation of the s-ethyl isomer of parathion was generally very rapid in all formulations studied. Dislodgable residues of paraoxon may be significant in some formulations and should be included in parathion degradation studies. Much of the parathion found on peach leaves throughout the growing season was dislodgable residue, but this depended considerably on the formulation used.

Biodegradation, Environmental↗
PubMed1979

Bioassay of parathion for possible carcinogenicity.

A bioassay for possible carcinogenicity of technical-grade parathion was conducted by administering the test chemical in the diet to Osborne-Mendel rats and B6C3F1 mice. Groups of 50 rats of each sex were administered parathion at one of two doses for 80 weeks, then observed for 32 or 33 weeks. Time-weighted average doses for males were 32 or 63 ppm; for females, they were 23 or 45 ppm. All surviving rats were killed at 112 or 113 weeks. Groups of 50 mice of each sex were administered parathion at one of two doses, either 80 or 160 ppm. The low-dose males were administered parathion for 71 weeks; the high-dose males for 62 weeks; and the low- and high-dose females for 80 weeks. The animals were then maintained for observation and all surviving mice were killed at 89 or 90 weeks. Matched controls consisted of groups of 10 untreated rats or mice of each sex; pooled controls of rats or mice taken from similar bioassays of other test chemicals were also used. Mean body weights of high-dose male and female rats and of high- and low-dose male mice were generally lower than those of the matched controls during the period of administration of the chemical. Mean body weights of the other groups of dosed rats and mice did not differ appreciably from those of the matched controls. Since body weights and survival of the female mice were not affected, female mice may have been able to tolerate a higher dose. Sufficient numbers of male and female animals of both species were at risk for the development of late-appearing tumors. In both male and female rats, the incidences of cortical adenomas or carcinomas of the adrenal showed dose-related trends (P<0.001) using pooled controls and, in direct comparisons, were higher in the high-dose groups (P<0.001) than in the pooled controls (males: pooled controls 3/80, matched controls 0/9, low-dose 7/49, high-dose 11/46; females: pooled controls 4/78, matched controls 1/10, low-dose 6/47, high-dose 13/42). Most of the tumors were adenomas. When the matched controls were used, dose-related trends in incidences of the adrenal tumors were significant (males, P=0.048; females, P=0.028); in direct comparisons, however, the incidences of the tumors in the individual groups did not differ significantly from those in corresponding matched controls. The incidences of the tumors in the dosed male and female rats were higher than those in corresponding historical controls (males 8/148, females 5/180). In mice, no tumors occurred in either sex at incidences that were significantly higher in the dosed groups than in the corresponding control groups. It is concluded that under the conditions of this bioassay, parathion was not carcinogenic to B6C3F1 mice. In the male and female Osborne-Mendel rats receiving parathion in their diet, there was a higher incidence of cortical tumors of the adrenal than in pooled or historical controls, suggesting that parathion is carcinogenic to this strain of rat.

Journal Article↗
PubMed1979

Sorption-desorption characteristics of methyl parathion by clays.

Methyl parathion (O,O-dimethyl O-(4-nitrophenyl) phosphorothioate) adsorption was studied on montmorillonite, kaolinite, halloysite, natural zeolite, ion exchange resins and calcium carbonate. Methyl parathion was highly adsorbed by montmorillonite, followed by zeolite, and very little adsorption was obtained on kaolinite and halloysite. Calcium carbonate did not exhibit any adsorption. The values of the partial molar free energy "delta G" were calculated for all systems. For the montmorillonite-methyl parathion system, the calculated partial molar heat of adsorption "delta H", and the conformity of the data to Freundlich equation indicated a possible physical mechanism of adsorption. Increasing acetone concentration decreases methyl parathion adsorption and dehydration increased adsorption in the nonaqueous system. Moreover, the increased adsorption on the swollen clay indicated that methyl parathion was adsorbed on the interlamellar surfaces of the clay. This was also in agreement with the results of the desorption studies, since the insecticide was not desorbed using the same aqueous acetone solution. This indicated that methyl parathion was adsorbed as a water-insoluble organic compound.

Adsorption↗
PubMed1988

The role of glutathione in the detoxification of the insecticides methyl parathion and azinphos-methyl in the mouse.

The dimethyl-substituted organothiophosphate insecticides methyl parathion and azinphos-methyl are thought to undergo glutathione-mediated detoxification in mammals. In the present study, depletion of hepatic glutathione in the mouse by pretreatment with diethyl maleate potentiated the acute toxicities of methyl parathion and azinphos-methyl, whereas depletion of hepatic glutathione by pretreatment with buthionine sulfoximine did not. Furthermore incubation of 50 microM methyl parathion with mouse hepatic microsomes for 5 min in the presence of 1 mM diethyl maleate led to significantly greater (p less than 0.05) production of methyl paraoxon, compared to incubations in the absence of diethyl maleate. Conversely, 1 mM diethyl maleate had no effect on metabolic activation of azinphos-methyl by mouse hepatic microsomes, while 10 mM inhibited slightly production of azinphos-methyl oxon from azinphos-methyl. These results suggest normal levels of hepatic glutathione are not required for detoxification of methyl parathion or azinphos-methyl in the mouse. Moreover the potentiation of the acute toxicity of methyl parathion following diethyl maleate pretreatment could result, at least in part, from enhanced production of methyl paraoxon. However, diethyl maleate likely acts through another mechanism(s) as well since it did not enhance the metabolic activation of azinphos-methyl in vitro. These data raise serious doubts about the participation of glutathione in the detoxification of methyl parathion and azinphos-methyl in vivo in the mouse.

Animals↗
PubMed1984

Kinetics of succinic dehydrogenase inhibition by methyl parathion and its recovery by oximes and L-cysteine in hepatopancreas of Lamellidens marginalis.

Effects in vitro of methyl parathion on some kinetic constants of succinic dehydrogenase (SDH) in hepatopancreas of freshwater mussel, L. marginalis were studied. Altered pH vs. specific activity curves for SDH demonstrated significant inhibition by methyl parathion in buffered acidic, neutral and alkaline ranges. At high pH ranges IC50 (12.5 microM) of methyl parathion did not cause 50% inhibition enzyme as it did at neutral and acidic pHs. Activation energies (delta E) were found to be increased suggesting decreased efficiency of enzyme in presence of methyl parathion. Non-competitive inhibition with respect to activation by succinate was indicated by decreased maximal velocity (V) without change in Michaelis Menten constant (Km). Pyridine-2-aldoxime (25 microM), pyridine-4-aldoxime (15 microM) and L-cysteine (40 microM) neutralized the inhibition of SDH by methyl parathion (12.5 microM). The kinetic data suggests that inhibition of SDH by methyl parathion was pH and temperature independent.

Animals↗
PubMed1975

Changes in cross-resistance spectrum resulting from methyl parathion selection of Culex tarsalis Coq.

Larvae of a field strain of Culex tarsalis Coq. manifesting a broad spectrum of resistance to organophosphorus (OP) insecticides were selected further by methyl parathion pressure in the laboratory. There was a 6.9 times further increase in resistance to methyl parathion in larvae, i.e., from 13.4 times level of resistance in the parental strain to 93.5 times level in the F11 generation. With the exception of fenthion and malathion, cross resistance in larvae the parental strain. The F11 larval population exhibited high levels of cross-resistance to chlorpyrifos (29.6 times), fenitrothion (49.4 times), parathion (55.6 times), fenthion (76.8 times), and chlorpyrifos-methyl (253.8 times). The high levels and broad spectrum of resistance to diverse OP compounds suggest the involvement of more than one mechanism in resistance. Larval selection also affected the spectrum of OP resistance in adults. The F11 adult population exhibited high levels of resistance to dichlorvos (48 times) and chlorpyrifos-methyl (40.1 times) insecticides propoxur, Mobam, Landrin or carbaryl, or to the chrysanthemate insecticide cismethrin. Resistance to the OP insecticides methyl parathion, parathion, fentirothion, fenthion and chlorpyrifos-methyl was found to be fairly stable over nine generations in the absence of methyl parathion selection pressure.

Animals↗
PubMed1995

A kinetic analysis of hepatic microsomal activation of parathion and chlorpyrifos in control and phenobarbital-treated rats.

A kinetic analysis of cytochrome P450-mediated desulfuration (activation) or dearylation (detoxication) showed that rat hepatic microsomes have a greater capacity to detoxify and a lower capacity to activate chlorpyrifos compared to parathion. Kinetic curves for the desulfuration of both parathion and chlorpyrifos were biphasic; Kmapps of 0.23 and 71.3 microM were calculated for parathion, and 1.64 and 50.4 microM for chlorpyrifos. While phenobarbital (PB) exposure seemed to generally lower the Kmapps for desulfuration except for the low Km activity on chlorpyrifos, the results were not statistically significant. While the low Km activity contributed 44 and 60% of the control Vmax for parathion and chlorpyrifos, respectively, it contributed 50 and 17% in PB-treated rats. These studies have indicated the presence of a low Km activity capable of functioning at very low substrate concentrations. A single dearylation Kmapp was calculated, 56.0 and 9.8 microM for parathion and chlorpyrifos, respectively. Phenobarbital exposure seemed to raise the Kmapps of dearylation; however, again, the results were not statistically significant. While numerous biochemical factors contribute to the overall toxicity levels of phosphorothionate insecticides, the in vitro efficiencies of hepatic microsomal desulfuration and dearylation of parathion and chlorpyrifos correspond to the acute toxicity levels.

Analysis of Variance↗
PubMed1996

Toxicokinetics of parathion and paraoxon in rainbow trout after intravascular administration and water exposure.

Fish are less sensitive than mammals to organophosphate insecticide toxicity. The species differences have been mainly investigated by biochemical studies of AChE and organophosphate interaction. To examine whether species differences in the toxicokinetics of the organophosphate insecticides were also involved in their differential toxicity, rainbow trout were fitted with a dorsal aorta cannula and administered parathion and its active metabolite paraoxon intraarterially (ia) and via water exposure. Serial blood samples were removed and the plasma concentrations of parathion and paraoxon were determined by capillary GC with EC detection. Plasma protein binding was determined by equilibrium dialysis and ultrafiltration. After ia injection the plasma concentration-time profiles of parathion and paraoxon were multiexponential, with a terminal t1/2 of 56.1 and 0.528 hr. The steady-state volumes of distribution and total body clearances (CLb) for parathion and paraoxon were 1370 and 1080 ml kg-1 and 21.4 and 3020 ml hr-1 kg-1; the plasma unbound fractions were 1.23 and 52.5%. The large difference in CLb between parathion and paraoxon appeared to result primarily from differences in plasma protein binding. Parathion had greater persistence in trout than rat, suggesting that sensitivity difference were unrelated to toxicokinetic differences.

Animals↗
PubMed1998

The effect of parathion on mouse testicular and epididymal development cultured in chicken allantochorion.

Parathion is a widely used organophosphoric pesticide which has also been reported to interfere with mouse spermatogenesis. Moreover it has been related to prenatal toxicity in mammals. Sixteen A/ Snell mice were sacrificed at day 17 of pregnancy. Testes and epididymides of the male fetuses were implanted in the allantochorion of chicken eggs. Three experimental conditions of the egg injections were considered: Group I: 1 ml of parathion (0.5 mg/ml), Group II: 1 ml of parathion (1 mg/ml), and Group III: 1 ml distilled water (control group). The implanted subjects continued their development for 4 days (i.e. to complete the gestational period for mice). The cell proliferation and differentiation of the epithelial cells of the epididymis were evaluated with the use of the monoclonal antiproliferating cell nuclear antigen (PCNA-cyclin) antibody, and the AE1 keratin complex antibody. Parathion altered the allantochorion, as 15% of the chicken embryos died in Group I and 40% in Group II, vs. only 8% in controls (Group III). However, no malformations were seen in the surviving embryos. In the testicular implants, the seminiferous cords of Group I had the same cytological characteristics of germ and pre-Sertoli cells as the control, except for involuting Leydig cells. Contrarily, in the cases with higher doses of parathion (Group II), there was a complete disorganisation of the seminiferous cords and the interstitium. In some testes, hyaline degeneration of the seminiferous cords was observed. No cell proliferation was evident, and the epididymal morphology was apparently unaffected. Therefore, parathion seems to interfere with normal testicular differentiation. However, in spite of interstitial damage, the epididymal development seems unaltered. Since the epididymis is an androgen-dependent organ, it may be postulated that testosterone production is still sufficient to support epididymal development but not spermatogenic cell line differentiation.

Allantois↗
PubMed1975

Studies on combined effects of organophosphates and heavy metals in birds. I. Plasma and brain cholinesterase in coturnix quail fed methyl mercury and orally dosed with parathion.

We found that mercury potentiated the toxicity and biochemical effects of parathion. Male Coturnix quail (Coturnix coturnix japonica) were fed a sublethal concentration of morsodren (4 ppm as methyl mercury) for 18 weeks. This resulted in an accumulation of 21.0 ppm of mercury in the liver and 8.4 ppm in the carcass. Birds fed clean feed and those fed morsodren-treated feed were orally dosed with 2, 4, 6, 8,and 10 mg/kg parathion, and their 48-h survival times compared. The computed LD50 was 5.86mg/kg in birds not fed morsodren and 4.24 in those fed the heavy metal. When challenged with a sublethal, oral dose of parathion (1.0 mg/kg), morsodren-fed birds exhibited significantly greater inhibition of plasma and brain cholinesterase activity than controls dosed with parathion. Brain cholinesterase activity was inhibited 41% in morsodren-fed birds and 26in clean-fed birds dosed with parathion, which suggested that the increase in parathion toxicity in the presence of morsodren was directly related to the inhibitation of brain cholinesterase.

Animals↗
PubMedDate not supplied

Methyl parathion increases neuronal activities in the rat locus coeruleus.

Exposure to organophosphate insecticides induces undesirable behavioral changes in humans, including anxiety and irritability, depression, cognitive disturbances and sleep disorders. Little information currently exists concerning the neural mechanisms underlying such behavioral changes. The brain stem locus coeruleus (LC) could be a mediator of organophosphate insecticide-induced behavioral toxicities since it contains high levels of acetylcholinesterase and is involved in the regulation of the sleep-wake cycle, attention, arousal, memory, and pathological processes, including anxiety and depression. In the present study, using a multi-wire recording technique, we examined the effects of methyl parathion, a commonly used organophosphate insecticide, on the firing patterns of LC neurons in rats. Systemic administration of a single dose of methyl parathion (1 mg/kg, i.v.) increased the spontaneous firing rates of LC neurons by 240% but did not change the temporal relationships among the activities of multiple LC neurons. This dose of methyl parathion induced a 50% decrease in blood acetylcholinesterase activity and a 48% decrease in LC acetylcholinesterase activity. The methyl parathion-induced excitation of LC neurons was reversed by administration of atropine sulfate, a muscarinic receptor antagonist, indicating an involvement of muscarinic receptors. The methyl parathion-induced increase in LC neuronal activity returned to normal within 30 min while the blood acetylcholinesterase activity remained inhibited for over 1 h. These data indicate that methyl parathion treatment can elicit excitation of LC neurons. Such excitation could contribute to the neuronal basis of organophosphate insecticide-induced behavioral changes in human.

Acetylcholinesterase↗