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)

In 25 years, at least eight of 50 total exposed employees in a small plant developed a mild neuropathy. Studies of urine or blood for lead, arsenic, mercury, cadmium, thallium, and antimony revealed no sign of toxic agents, but the atmosphere in one room contained toxic levels of n-hexane. The sourse was the glue used in the plant. Serum cholinesterase levels were reduced, offering a possible laboratory tests to alert clinicians to the possibility of n-hexane exposure. All patients recovered completely. Mechanical and administrative adjustments should prevent such industrial accidents.
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PMID:Polyneuropathy due to n-hexane. 18 98

This study describes an outbreak of polyneuropathies in an artificial leather shoe factory. Thirty-seven females employed in the factory were examined; clinical findings and hematochemical data suggest a possible role of tricresylphosphate (TCP) in the genesis of these polyneuropathies. A high percentage of subjects evidenced definite signs of upper-motor neuron involvement, which appeared at an early or late stage of the disease. A statistically significant (P less than .001) reduction of red-blood-cell acetylcholinesterase (AChE) was found in the subjects. The ascertained upper-motor neuron involvement suggests a connection with previously described intoxications by TCP- by ingestion or occupational poisoning. The reduction of AChE seems attributable to TCP, and not to n-hexane, whose anti-AChE activity has never been demonstrated.
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PMID:Polyneuritis incidence in shoe factory workers: cases report and etiological considerations. 68 46

Hydrophobity (coefficient in distribution in the hexane water system) and the content of cholinesterase organophosphorous inhibitors (OPI) of the structure Ro (CH3) P (O) SC2H4 SC2H5 were studied in the rat brain. When the O-alkyl radical is increased hydrophobity rises and the relative content of free OPI in the brain extracted by chloroform decreases. With an increase in R from the ethyl to butyl one the ability to the additional inhibition of the brain own cholinesterase lowers due to incubation of homogenate at 37 degrees C, that evidences for an essential drop in the studied series of the free OPI fraction relative to the free OPI extracted by chloroform.
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PMID:[Binding of phosphoorganic cholinesterase inhibitors in rat brain tissue]. 98 15

The article deals with the hydrophobic character (distribution coefficient in the systems hexane - water and chloroform - water) and certain peculiarities of distributing three cation-containing phosphoroganic inhibitors of cholinesterase and their uncharged analogues in the organisms. The distribution coefficients in the charged and uncharged compounds in the system hexane - water differ inconsiderably, whereas in the system chloroform-water by the thousands and millions times. In rabbits with intravenous administration the content of all inhibitors in blood decreases rapidly, the uncharged compounds accumulate selectively in the lungs and the charged ones are distributed evenly in the tissues.
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PMID:[The distribution of cholinesterase charged phosphorganic inhibitors and their uncharged analogues in tissues]. 120 7

The effects of toluene and n-hexane on rat synaptosomal membrane fluidity and the integral enzymes acetylcholinesterase (AChE) and ATPase were studied in vitro. The synaptosome membranes were isolated in Percoll and sucrose gradients. After adding toluene and n-hexane to the incubation mixture (37 degrees) in 2,4,6 and 8 mM concentrations, the fluidity changes were measured by the lateral pyrene diffusion method from Percoll-isolated membranes, and the ATPase and acetylcholinesterase activities were determined from both synaptosome isolations. Addition of toluene caused a linearly correlated increase of the synaptosomal membrane fluidity and a linear decrease of the AChE activity. The ATPase activity did not decrease linearly but dose-dependently. In contrast to the effects of toluene in vitro, addition of n-hexane in the same concentration range had no comparable influence on membrane fluidity nor on the activities of both integral enzymes despite its even higher lipid/water partition coefficient. Toluene increases synaptosomal membrane fluidity and at the same time inhibits the integral enzymes, probably by disturbing the lipid/protein interaction.
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PMID:Effects of toluene and n-hexane on rat synaptosomal membrane fluidity and integral enzyme activities. 144 47

The joint neurotoxic action of simultaneous exposure to vapors of n-hexane and methyl iso-butyl ketone (MiBK) and dermally applied O-ethyl O-nitrophenyl phenylphosphonothioate (EPN) was studied in groups of five adult hens. Four groups of hens were concurrently exposed to a dermal 2.5 mg/kg of EPN, 1000 ppm of n-hexane and 100, 250, 500 or 1000 ppm of MiBK. Two groups were each exposed to binary mixtures of a dermal dose of 2.5 mg/kg of EPN and 250 ppm of MiBK or 1000 ppm of n-hexane. Another three groups of hens were exposed to either 250 ppm of MiBK, 1000 ppm of n-hexane or a dermal dose of 2.5 mg/kg of EPN. A Group of hens was kept untreated. All hens were terminated after 30 days of treatment. Hens exposed to MiBK or n-hexane vapor did not exhibit any toxicity signs. In contrast, hens treated with EPN alone or in combination with n-hexane and/or MiBK developed acute cholinergic and delayed neurotoxicity signs. Hen brain acetylcholinesterase and neurotoxic esterase activities were inhibited in hens treated concurrently with EPN, n-hexane and MiBK. MiBK alone or in combination with EPN and n-hexane induced liver microsomal cytochrome P-450 content and phenobarbital-inducible cytochrome P-450 enzyme activities. Microsomes from hens treated with EPN, n-hexane, MiBK or mixtures of EPN, n-hexane and MiBK significantly enhanced the biotransformation of EPN to the more neurotoxic oxidation metabolite O-ethyl O-4-nitrophenyl phenylphosphonate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of joint neurotoxicity of n-hexane, methyl isobutyl ketone and O-ethyl O-4-nitrophenyl phenylphosphonothioate in hens. 201 92

This article reviews the biological indicators available for monitoring human neurotoxicity by exogenous chemicals with reference to the phases in which the neurotoxic process takes place, namely delivery, receptor-linkage, and toxicodynamic phase. Among the delivery phase tests, indicators are available for metals (lead, mercury) and some organic substances (CS2, n-hexane, DDT, etc.), but a correlation between neurotoxic effects and these indices is rather loose or not yet proved. The receptor-phase tests comprise well known enzymes, such as cholinesterase, less known but promising indicators, such as neuropathy target esterase (NTE), and new tools under study, such as acrylamide-hemoglobin adducts or 2,5-hexanedione-protein adducts. The toxicodynamic phase tests, which mainly consist of measuring substances released from the nervous system, have provided so far rather poor results, but more specific techniques of measurement (monoclonal antibodies) could offer new possibilities in the future.
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PMID:Biological indicators of neurotoxicity in central and peripheral toxic neuropathies. 307 8

Adult male rats were subjected to 4 weeks' respiratory treatment with n-hexane (5000 ppm, 16h/day, 6 days/week); motor conduction velocity was significantly decreased in tail nerves at all weekly intervals and did not approach normal values in the 4 weeks following interruption of treatment. Plasma acetylcholinesterase (AChE) levels were significantly increased at all weekly intervals during treatment (25-40%); 2 weeks after the end of treatment they had returned to baseline. Oral treatment with 2,5-hexanedione (HD) (1% in drinking water) caused a similar increase in plasma levels; this increase was statistically significant also when compared with pair-fed (PF) control rats. A sucrose density gradient analysis showed only one peak of AChE activity at approximately 10 S (as in normal plasma). The levels of butyrylcholinesterase were unaltered in plasma of both n-hexane-and HD-treated rats. Both the fast-contracting EDL and the slow-contracting soleus muscles lost weight in HD-treated rats with respect to free-fed (AL) and PF controls. AChE levels responded differently to HD treatment in the two muscle types: in EDL total extracts, AChE activity increased considerably with respect to AL controls (+ 70%, p less than 0.001), while the levels of the 16 S and 4 S molecular forms were unaltered. The increased levels of AChE found in plasma of rats intoxicated with n-hexane or with its metabolite HD may originate from muscle and correspond to an increased secretion of this molecular form.
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PMID:Cholinesterases in blood plasma and tissues of rats treated with n-hexane or with its neurotoxic metabolite 2,5-hexanedione. 343 86

Commercial hexane was concentrated by distillation. The distillation residue (0.43 ml/l original solvent) contains material which inhibits human serum cholinesterase (ChE) "in vitro" with a slight effect on acetylcholinesterase. Phosphorus was detected equivalent to 0.33 mumol monophosphorus compound/litre original solvent. The inhibition was progressive with the enzyme-inhibitor preincubation time. A partial reactivation of the inhibited enzyme was obtained by treatment with hydroxylamine and 2-PAM. The results are coherent with a covalent inactivation by more than one inhibitor which acylate (probably phosphorylate) ChE, although it seems likely that a reversible but unstable inhibitor could also be present in the hexane residue. The results are discussed in the context of the known neurotoxic effects of n-hexane and some organophosphorus esters.
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PMID:Serum cholinesterase inhibitors in the commercial hexane impurities. 688 13

The toxic effects of i.p. administered n-hexane and n-heptane on biochemical processes in rat liver, as indicated by the increase in alkaline phosphatase activity and decrease in FDP aldolase activity, and their reflection on blood chemistry, were studied. Serum cholinesterase activity and albumin and cholesterol content showed statistically significant decreases with the increase in FDP aldolase activity. The significance of the findings is discussed.
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PMID:Toxicity of n-hexane and n-heptane: some biochemical changes in liver and serum. 716 75


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