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At least 19 recordsLinked to original sources
PubMedDate not supplied

Biotransformation of the organophosphorus insecticides parathion and methyl parathion in male and female rat livers perfused in situ.

Although numerous previous reports have characterized the mammalian biotransformation of the organophosphorus insecticides parathion and methyl parathion, questions still remain regarding the toxicological significance of certain metabolic pathways in vivo. The present study utilized rat liver perfusions in order to better characterize the hepatic biotransformation of parathion and methyl parathion in intact liver. Single-pass liver perfusions with parathion and methyl parathion over a range of perfusate concentrations of 10-80 microM resulted in the appearance of paraoxon and methyl paraoxon, respectively, in effluent. Furthermore, rat blood did not have the capacity to prevent transport of paraoxon and methyl paraoxon to extrahepatic tissues, suggesting that oxon produced hepatically can distribute to extrahepatic tissues. In addition, striking sex differences were noted in the metabolite profile of parathion and methyl parathion in perfused livers. However, these differences could not account for the observation that females are more susceptible to parathion, but less susceptible to methyl parathion, compared to males. And finally, S-methyl glutathione or S-p-nitrophenyl glutathione could not be detected in effluent or bile of livers from either sex perfused with methyl parathion, suggesting that glutathione-dependent detoxification of this insecticide does not occur to any significant degree in intact rat liver.

Animals↗
PubMed1985

Effect of serum-parathion interactions on cutaneous penetration of parathion in vitro.

The effect of serum and serum fractions on the cutaneous penetration of [35S]parathion from surface deposits or adsorbed formulations was determined. The total quantity of [35S]parathion which penetrated pig skin was significantly greater when the receptor fluid was whole swine serum or the 500 or 10,000 MW retentate from ultrafiltration of the serum than when phosphate-buffered saline (PBSA), the 500 MW filtrate or distilled water, respectively, was used. The enhanced penetration was observed without any associated evidence of metabolic change and with both dosing methods. This result is consistent with the hypothesis that serum-parathion interactions are the cause of the enhanced penetration. The apparent solubility of parathion was 16 times greater in whole serum than in PBSA. Gel-filtration chromatography of the serum-parathion mixture revealed that approximately 11% of the 35S activity was associated with two protein fractions which had consistently different elution volumes. Most of the radioactivity, however, was not tightly bound and the equilibrium between bound and free parathion was rapidly reversible. The result of interaction between parathion and serum proteins was an increased apparent solubility, relative to PBSA, and increased cutaneous penetration. The significance of these findings is clear: when designing in vitro systems to model in vivo percutaneous absorption, investigators should consider that the affinity of the fluid interfacing with the dermis in vivo may influence the kinetics of penetration when subcutaneous blood flow is low.

Animals↗
PubMed1992

Prolonged toxicity with intermediate syndrome after combined parathion and methyl parathion poisoning.

A prolonged type of organophosphate toxicity, previously characterized as the Intermediate Syndrome, has been recognized in 6 out of 7 prospectively studied patients poisoned by insecticide containing parathion and methyl parathion in equal proportions. The clinical characteristics included respiratory paresis, weakness in the territories of several motor cranial nerves, neck flexors and proximal limb muscles, and depressed tendon reflexes, all lasting for several days or weeks. Electromyography in the early stages disclosed diverse types of impaired neuromuscular transmission. EMG normalization preceded clinical recovery. Severe plasma butyrylcholinesterase and erythrocyte acetylcholinesterase inhibition persisted along with the occurrence of Intermediate Syndrome-related symptoms. We conclude that combined parathion and methyl parathion poisoning is more likely to induce Intermediate Syndrome than parathion poisoning alone. The mechanisms underlying this difference remain obscure. The Intermediate Syndrome shows clinical and electromyographic hallmarks of combined postsynaptic impairment of neuromuscular transmission.

Adult↗
PubMedDate not supplied

The role of the liver in mediating the acute toxicity of the pesticide methyl parathion in the mouse.

Mouse livers perfused in situ with the pesticide methyl parathion (O,O-dimethyl O-P-nitrophenyl phosphorothioate) resulted in the appearance of the toxic metabolite, methyl paraoxon (O,O-dimethyl-O-P-nitrophenyl phosphate), in the effluent perfusate. Mouse whole blood rapidly detoxified methyl paraoxon in vitro, but not at a rate sufficient to prevent transport of at least some of this toxic metabolite from liver to other tissues in vivo. The hepatic disposition and biotransformation of methyl parathion in perfused livers were altered markedly by changes in protein binding of methyl parathion to perfusate, but only slightly by changes in perfusate flow rates that maintained viable livers. Pretreatment of mice with phenobarbital daily for 4 days (80 mg/kg, ip) induced hepatic microsomal activation of methyl parathion to methyl paraoxon in vitro and increased the clearance of methyl parathion by perfused mouse livers. However, in contrast to perfusion of methyl parathion into livers from saline-pretreated mice, perfusion of methyl parathion into livers from phenobarbital-pretreated mice did not lead to the appearance of methyl paraoxon in effluent perfusate. Nevertheless, methyl paraoxon was produced intrahepatically during these perfusions since hepatic cholinesterase activities were depressed compared to livers from phenobarbital-pretreated mice perfused without methyl parathion. Furthermore, phenobarbital pretreatment antagonized the acute toxicity of methyl parathion in vivo in the mouse. These data demonstrate that the net result of the biotransformation of methyl parathion by livers in untreated mice is metabolic activation, whereas the net result by livers of phenobarbital-pretreated mice is detoxification.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗