Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.7 (acetylcholinesterase)
28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mipafox administered to rats daily for 35 days produced ataxia and a reduction in the level of dopamine in the corpus striatum. Treatment with Leptophos for the same period produced slight motor dysfunction and a small but significant reduction in the level of striatal dopamine. Fenitrothion neither produced motor dysfunction nor changed the level of striatal dopamine. The cholinesterase activity of corpus striatum was inhibited by all the compounds. The results suggest the possible involvement of striatal dopamine in the delayed neurotoxic effects of certain organophosphorus compounds.
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PMID:Role of striatal dopamine in delayed neurotoxic effects of organophosphorus compounds. 5 73

Phosfolan, chlorpyrifos, and stirophos when applied to white mice at sublethal doses did not induce any delayed neurotoxic effect. On the other hand, Leptophos and EPN when administered orally at sublethal or lethal levels clearly produced a delayed neurotoxic ataxia in treated mice. The five tested organophosphorus insecticides were compared for their ability to inhibit cholinesterase, neurotoxic esterases and monoamine oxidase. I50 values were estimated for each case. The results revealed that all five compounds were inhibitors of cholinesterase, but only Leptophos and EPN were shown to be potent inhibitors for both neurotoxic esterase and monoamine oxidase in the mouse brain. Additional particular properties of both Leptophos and EPN were found in their ability to cause delayed neurotoxic ataxia in chickens and sheep fed once on sublethal doses of these compounds. It is believed that the phosphonate ester configuration of EPN and Leptophos has a specific mode of toxic action which is mainly located at the central nervous system. It is also postulated that these delayed neurotoxic agents might inhibit postganglionic sympathetic neurons, thus resulting in chronic paralytic effects.
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PMID:Neurotoxicity of organophosphorus insecticides Leptophos and EPN. 7 68

Leptophos (O-[4-bromo-2,5 dichlorophenyl] O-methyl phenylphosphonothioate) (PhosvelR) was administered orally to chickens and rats in doses of 0.5 and 5.0 mg/kg/day for 26 weeks. Hens fed 5.0 mg/kg, except one, showed ataxia and became paralysed in the legs at varying times from 8 to 19 weeks. A fifth hen showed ataxia early in the experiment but recovered fully for the remainder of the experiment. Rats fed both doses and chickens fed 0.5 mg/kg showed no signs of delayed neurotoxicity. All hens fed 5.0 mg/kg stopped laying by about the third week. Animals of both species fed 5.0 mg/kg either lost weight (chickens) or gained less weight (rats) than the others. Erythrocyte acetylcholinesterase (AChE) of the chickens given both doses was significantly depressed at first, then increased, and later dropped to control levels. AChE of rats fed 0.5 mg/kg was significantly inhibited but soon recovered to within control levels. On the other hand, the AChE of rats fed 5.0 mg/kg was inhibited throughout the experiment. Plasma cholinesterase (ChE) of both species was first inhibited and then recovered erratically for both insecticide concentrations. Histological alterations in the spinal cord of paralysed hens included axon and myelin degeneration in the ventral, lateral and posterior columns. In the paralysed hens, 79% of the neurotoxic esterase in the brain were inhibited, whereas in the non-paralysed hens (including the one non-paralysed hen receiving 5.0 mg/kg/day) and all rats only about half as much was inhibited.
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PMID:Neurotoxic effects of leptophos (PhosvelR) in chickens and rats following chronic low-level feeding. 8 38

Ataxia and depression developed in 21 of 50 (42%) laboratory cats wearing flea collars impregnated with 2,2-dichlorovinyl dimethyl phosphate (dichlorvos or DDVP) in a warm dry environment. Five (10%) of the cats died. Whole blood cholinesterase (ChE) activity was significantly (P smaller than 0.001) reduced in all cats and cervical dermatitis occurred in 37 (74%) of them.
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PMID:Ataxia, depression, and dermatitis associated with the use of dichlorvos-impregnated collars in the laboratory cat. 123 42

This study examined the effects of the organophosphorus delayed neurotoxicant bis (1-methylethyl) phosphorofluoridate (DFP) on the central nervous system of the European ferret. Animals received subcutaneous injections of either 2 or 4 mg DFP/kg b.w. The extent of neuropathology was determined by the Fink-Heimer method, the activities of neuropathy target esterase (NTE) and cholinesterase (ChE) by enzyme assay methods, and the severity of clinical signs by a graded scale. In ferrets injected with 4 mg DFP/kg b.w., dense axonal and terminal degeneration were noted at 21 and 28 days post-DFP in the gracile, inferior vestibular, and lateral reticular nuclei, medial and dorsal accessory nuclei of the inferior olive, and in cerebellar folia I-IV. Degeneration was also noted in laminae VI-VII throughout most of the spinal cord and in the ventral motor nucleus at the level of the cervical enlargement. Both NTE and ChE activities were maximally inhibited at 6 hr post-dosing. NTE activity returned to control levels by 4 days while ChE activities reached control levels at 21 days. Clinical signs at 21 and 28 days post-DFP ranged from slight hindlimb weakness to severe ataxia or hindlimb paralysis. Less severe degeneration and clinical signs were noted in the animals exposed to 2 mg DFP/kg b.w. These findings indicate that the European ferret may be a model species for assessing the effects of organophosphorus delayed neurotoxicants.
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PMID:Delayed neurotoxic effects of bis (1-methylethyl) phosphorofluoridate (DFP) in the European ferret: a possible mammalian model for organophosphorus-induced delayed neurotoxicity. 195 82

Cerebrospinal fluid (CSF) amino acid neurotransmitters, related compounds, and their precursors, choline levels, and acetylcholinesterase activity were measured in the CSF of patients with cerebellar ataxia during a randomized, double-blind, crossover, placebo-controlled clinical trial of physostigmine salicylate. The CSF gamma-aminobutyric acid, methionine, and choline levels, adjusted for age, were significantly lower in patients with cerebellar ataxia compared with controls. Physostigmine selectively reduced the level of CSF isoleucine and elevated the levels of phosphoethanolamine. No change occurred in CSF acetylcholinesterase activity and in the levels of plasma amino compounds in patients with cerebellar ataxia when compared with controls. Median ataxia scores did not statistically differ between placebo and physostigmine nor did functional improvement occur in any of the patients.
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PMID:Cerebrospinal fluid as a reflector of central cholinergic and amino acid neurotransmitter activity in cerebellar ataxia. 197 60

Utilizing a variation of the Fink-Heimer method, we examined the extent and location of axonal and terminal degeneration within the chicken cervical spinal cord, brainstem and cerebellum resulting from a single subcutaneous dose of bis(1-methylethyl)phosphorofluoridate (DFP). The effects of DFP on the activities of whole-brain neuropathy target esterase (NTE) and cholinesterase (ChE) were also assessed as were the development and severity of clinical signs characteristic of organophosphorus-induced delayed neuropathy (OPIDN). Both whole brain NTE and ChE activities were maximally inhibited during the first 24 h post-exposure, showing gradual recovery over a period of 3 weeks. OPIDN clinical signs were not observed at 7 days post-DFP but progressed to severe ataxia by day 14 and paralysis by day 21. There was a relative absence of degeneration at 7 days, a dramatic increase in degeneration density at 14 days, and high density degeneration at both 21 and 28 days. Cervical spinal and medullary tracts containing axonal degeneration included the fasciculus gracilis, dorsal and ventral spinocerebellar tracts, spinal lemniscus, and the intramedullary portions of the glossopharyngeal and vagus nerves. Brainstem nuclei containing terminal degeneration included the lateral cervical, gracile-cuneate, external cuneate, and inferior olivary nuclei, the nucleus tractus solitarius, and the lateral and paragigantocellular lateral reticular nuclei. Mossy fiber degeneration was also present in cerebellar folia I-Vb. These results show that exposure to DFP causes axonal and terminal degeneration in ascending spinal tracts, brainstem nuclei and cerebellar folia associated with the transmission of somatic and visceral sensory information.
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PMID:Selective axonal and terminal degeneration in the chicken brainstem and cerebellum following exposure to bis(1-methylethyl)phosphorofluoridate (DFP). 239 6

The effects of desbromoleptophos, fenitrothion, and fenthion on brain acetylcholinesterase (AChE), brain neurotoxic esterase (NTE), and walking were investigated in immature chicks, below the age of organophosphorus ester-induced delayed neurotoxicity (OPIDN). Seventy-five milligrams per kilogram of the delayed neurotoxicant desbromoleptophos (DBL) and 100 mg/kg of the nonneurotoxicant fenithrothion (FTR) were given orally to 8-d-old chicks. Five milligrams per kilogram of the suspected neurotoxicant fenthion (FEN) was administered topically for 7 d, in 4 different age groups. Behavioral testing was performed for treated and control chicks on various days after treatment. Brain NTE and AChE assays were carried out for treated and control chicks on each day of behavioral testing. NTE and AChE inhibition were around 80 and 50%, respectively, 24 h after treatment, for the chicks treated with DBL. NTE returned to normal levels by 20 d and AChE by 6 d after treatment. FTR caused 56% AChE inhibition but not NTE inhibition 24 h after treatment. NTE inhibition for the FEN-treated chicks never exceeded 25% during the whole period of the experiment, whereas 65 and 54% inhibition of AChE was seen in two age groups. DBL and FEN significantly altered the gait of treated chicks, but the non-OPIDN-inducing FTR did not. FEN-treated chicks developed an atypical ataxia at the normal age for onset of sensitivity to OPIDN. Minimal NTE inhibition, long latency for the development of ataxia, and immaturity of the chicks at treatment distinguish FEN-induced functional deficits from classical OPIDN.
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PMID:Acute and delayed effects of fenthion in young chicks. 243 99

Certain biochemical and behavioral effects of carbaryl were investigated in chicks. Six-day-old birds received 100 mg/kg body weight (bw) per day carbaryl for 7 d. Brain acetylcholinesterase (AChE) and neuropathy target esterase (NTE) were measured at 24 h after the first, third, and fifth dose during the 1 wk of treatment, and then at d 1, 3, 6, 10, 20, 30, and 40 after the last dose. Gait analysis was evaluated on each posttreatment day. No significant reduction in both NTE and AChE activities was noticed throughout the experiment. However, carbaryl altered the locomotion of the chicks from d 1 until d 40 after last treatment. The stride length of the treated birds was significantly shorter than that of the controls. A significant increase in the stride width and sine of the angle of placement was noticeable throughout the period of the experiment. Thus, treated chicks walked with abnormal gait. Delayed ataxia and paralysis occurred 20 d after the last treatment and lasted until the end of the experiment or eventually death.
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PMID:Enzyme and behavioral changes in young chicks as a result of carbaryl treatment. 249 47

Organophosphate-induced delayed polyneuropathy (OPIDP) is initiated by inhibition/aging of more than 70-75% of neuropathy target esterase (NTE). Di-n-butyl-2,2-dichlorovinyl phosphate (DBDCVP) (1 mg/kg s.c.) inhibited 96%, 86% and 83% of NTE in brain, spinal cord and peripheral nerve, respectively, and induced a typical central peripheral distal axonopathy in hens. A lower dose (0.45 mg/kg s.c.) caused 90%, 83% and 54% NTE inhibition in the same organs; by contrast, hens developed a spastic ataxia with axonal degeneration in spinal cord but not in peripheral nerve. With a dose of 0.2 mg/kg s.c., a suprathreshold inhibition of NTE was produced in brain (78%) but not in spinal cord (56%) and peripheral nerve (33%) and no morphological or clinical signs of neuropathy developed in hens. With doses up to 4.0 mg/kg s.c., acetylcholinesterase (AChE) inhibition was similar throughout the nervous system. In vitro time-course inhibition studies showed a different sensitivity to DBDCVP of NTE from peripheral nerve (ka = 5.4 x 10(6)) relative to that from spinal cord (ka = 13.9 x 10(6)) or brain (ka = 20.6 x 10(6)). In vitro I50s of DBDCVP for AChE were similar in brain, spinal cord and peripheral nerve (11-17 nM). These data support the hypothesis that the critical target for initiation of OPIDP is located in the nerve fiber, possibly in the axon and also suggest that peripheral nerve NTE has a different sensitivity to DBDCVP than the brain enzyme.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vivo and in vitro regional differential sensitivity of neuropathy target esterase to di-n-butyl-2,2-dichlorovinyl phosphate. 261 60


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