Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When an automated counting instrument using an esterase stain was employed, decreased monocyte counts were observed in a group of process workers exposed to organophosphate esters. Their monocyte counts were not found to be depressed with manual counting or with an automated counter using another staining method. The apparent depression was transient. In these workers and a comparison group, theoretical adverse consequences of decreased monocyte esterase and also possible changes in other esterases were explored. No anergy was seen with mumps or staphylococcal phage lysate hypersensitivity skin tests. Histology of the mumps reaction was similar in both groups. The depressed monocyte counts were significantly associated with a mild reduction in erythrocyte cell acetylcholinesterase, but no reduction was seen in plasma pseudocholinesterase or lymphocyte neurotoxic esterase.
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PMID:Industrial exposure to organophosphorus compounds. Studies of a group of workers with a decrease in esterase-staining monocytes. 241 79

An aerosol preparation containing 2.5% chlorpyrifos was applied to the tail and umbilicus of newborn pigs. Mortality was 7/7 pigs treated 0-3 hr after birth, 3/5 pigs treated at 24-30 hr, and 0/3 pigs treated 30-36 hr after birth. Clinical signs consistent with organophosphate (OP) toxicosis were demonstrated by pigs that subsequently died or were euthanatized in extremis. Blood and brain cholinesterase (ChE) activities were depressed in affected pigs compared to controls. Only 1/3 pigs treated 30-36 hr after birth had a diagnostically significant depression in blood ChE. These results indicate that piglets one day or less of age are susceptible to OP toxicosis by cutaneous absorption of chlorpyrifos.
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PMID:Age related susceptibility of newborn pigs to the cutaneous application of chlorpyrifos. 242 59

1. The amplitudes of end-plate currents (EPCs) evoked by stimulating the nerve with frequencies ranging from 1 to 5 Hz and the amplitudes of miniature end-plate currents (MEPCs) gradually diminish if choline uptake is blocked by hemicholinium-3 (HC-3, 20 microM). This reduction of EPC amplitudes is predominantly of presynaptic origin, although an observed decrease in MEPC amplitudes suggests that some postsynaptic changes [due to direct action of HC-3 on acetylcholine (ACh) receptors or on open ACh channels] also occurs. 2. Shortening of both EPCs and MEPCs is observed during high-frequency stimulation (5 Hz) in the presence of cholinesterase inhibitor after impairment of ACh synthesis. Shortening of MEPCs probably results from a direct blocking action of HC-3 on open ACh channels, as well as from reduction in quantal size. Shortening of EPCs is more pronounced (EPCs eventually have shorter time courses than MEPCs) and usually does not result from a gradual reduction in the spatial overlap of quantal events (because of reduced quantal content) or from a diminished 'lingering ACh' (ACh that remains in the synaptic cleft between nerve impulses), but rather from a much reduced quantal size of nerve-evoked quanta. 3. It therefore appears that the quanta that are released by nerve stimulation are preferentially filled with newly synthesized ACh. In its absence nerve stimulation leads to secretion of only partially filled quanta. This occurs simultaneously with spontaneous secretion of almost normally filled quanta. Hence it seems that the quantal discharge is not strongly dependent, if at all, on its ACh content. Moreover, the correspondence between the quantal sizes of nerve-evoked and spontaneously released quanta does not remain valid during high-frequency prolonged stimulation. 4. Even with the choline uptake system intact, prolonged high-frequency stimulation leads to a gradual shortening of EPCs and, to a small extent, MEPCs. Shortening of EPCs appears to be mainly a result of a reduction of their quantal size. 5. It is estimated from the shortening of EPCs and the known EPC versus MEPC relationship that the reduction of the quantal sizes of nerve-evoked quanta probably contributes very significantly to synaptic depression that occurs during prolonged high-frequency nerve stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Synaptic depression in frog neuromuscular junction. 244 Oct 3

Interactions of the oximes pyridine-2-aldoxime (2-PAM) and 1-(2-hydroxyiminomethyl-1-pyridino)-3-(4-carbamoyl-1-pyridino++ +)-2-oxapropane dichloride (HI-6), reactivators of phosphorylated acetylcholinesterase enzyme, with the nicotinic acetylcholine receptor-ion channel complex were studied using electrophysiological techniques. Single channel studies revealed that both oximes increased the opening probability of channels that were activated by acetylcholine. The oximes reduced mean channel open time and burst time in a concentration- and voltage-dependent manner. End-plate current amplitude was increased by 2-PAM (10-100 microM) and HI-6 (1 microM) but depressed at higher concentrations of these agents. The oximes decreased the time constant of end-plate current decay, particularly at hyperpolarized membrane potentials. HI-6 depressed indirect twitch response of the sartorius muscle, whereas 2-PAM caused a facilitation followed by depression. Both agents directly hydrolyzed acetylthiocholine, in addition to weakly inhibiting acetylcholinesterase. Our study demonstrates a direct molecular interaction of the oximes HI-6 and 2-PAM with the natural agonist molecule and with the acetylcholine receptor-ion channel complex. These effects can explain the excitatory and inhibitory actions of both agents, and may form the basis for their antidotal effectiveness against organophosphorus poisoning. The quantitative differences between the effects of 2-PAM and HI-6 on the above parameters are important in view of their differential antidotal efficacies.
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PMID:Acetylcholinesterase reactivators modify the functional properties of the nicotinic acetylcholine receptor ion channel. 245 74

Mivacurium is a new short-acting competitive neuromuscular blocking agent. Infusion requirements for the maintenance of a stable 90-99% muscle twitch depression were determined in 28 children anaesthetized with nitrous oxide and 1% halothane (inspired) in oxygen or nitrous oxide in oxygen and opioid. Neuromuscular block was assessed by monitoring the force of contraction of the adductor of the thumb during train-of-four (TOF) stimulation at 0.1 Hz. Infusion rate and twitch depression were analysed from 15 to 75 min and from 75 to 135 min after the start of the infusion. In the first period of evaluation, the mean infusion requirement was 10.4 (SEM 0.92) micrograms kg-1 min-1 during the halothane anaesthesia and 13 (1.4) micrograms kg-1 min-1 during the opiod anaesthesia (P less than 0.05). This difference was present also during the second 60-min period. There was no significant correlation between infusion rates required to maintain greater than 90% depression of the first twitch (T1) of the TOF and plasma cholinesterase concentrations. Regardless of the anaesthetic regimen, children recovered rapidly after discontinuing the infusion. The recovery index (25-75% recovery of T1) for all patients was 5.4 (0.57) min with no significant differences between the groups.
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PMID:Continuous infusion of mivacurium in children. 253 33

The effects of lethal (2.0 mg/kg) and high sublethal (1.3 mg/kg) dosages of the organophosphate acetylcholinesterase (AChE) inhibitor paraoxon on FR10 performance rate was determined 1 and 2 days after intoxication. The lethal doses were antidoted with either centrally acting atropine sulfate (AS), or atropine methyl bromide (AMB) or atropine methyl nitrate (AMN), both quaternary salts and not expected to act centrally. AChE inhibition in the brain was about 35-60% on the second day after treatment. AS yielded a small transient depression in performance, while AMB and AMN yielded severe deficits, with incomplete recovery. Performance was depressed by 1.3 mg/kg paraoxon by 52% and 34% on days 1 and 2, respectively, while performance was more greatly depressed by the lethal dose, especially with the noncentrally acting antidotes: AS, 67 and 48%; AMB, 81 and 55%; AMN, 91 and 78%. However, a low dose of AS with 2 mg/kg paraoxon resulted in very severe, nonrecovering deficits. A lethal dose of the nonpersistent anti-AChE eserine sulfate, antidoted with a low dose of AS, yielded no deficits. Thus, a high level, acute intoxication with paraoxon yields behavioral deficits which are attenuated by high levels of a centrally acting muscarinic receptor antagonist. The paraoxon-induced performance deficits or their recovery do not correlate directly with AChE inhibition.
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PMID:Short-term effects of paraoxon and atropine on schedule-controlled behavior in rats. 259 81

1. The amplitudes of end-plate currents (EPCs) in short trains of fifteen to seventeen EPCs at 10 Hz were depressed in the presence of 10 microM-proadifen when acetylcholinesterase (AChE) was inhibited. 2. The proadifen-induced EPC depression was voltage-dependent and the effect was more pronounced at negative membrane potentials. 3. In the presence of proadifen, the mean amplitude of miniature end-plate currents (MEPCs) was reduced by 36% 5 s after the EPC train as compared with MEPCs before the train. 4. Without proadifen, but with inhibited AChE, an increase of temperature from 20 to 26 degrees C and elevation of external Ca2+ from 1.8 to 2.5 mM led to EPC amplitude depression in the train, which was also potential-dependent. 5. After AChE inhibition, proadifen (10 microM) progressively shortened MEPC decay without significant reduction of amplitude up to 40 min of exposition. MEPCs were not affected by proadifen when AChE was active. 6. It is concluded that these postsynaptic effects of proadifen can be explained neither by its action on the resting acetylcholine receptors (AChR) nor on open ion channels but are due to its desensitization-promoting action.
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PMID:Development of desensitization during repetitive end-plate activity and single end-plate currents in frog muscle. 260 Aug 28

In this paper the activity of blood cholinesterase and serum cholinesterase were reported in 32 depressions without physical disease. There were 20 males and 12 females. Prior to study none of the patients received antidepressants, lithium and antipsychotics or other therapies. The control group consisted of 43 normal healthy persons (male: 32, female: 11). The results showed that the mean activity unit of blood cholinesterase and serum cholinesterase were lower in major depression than in the control group. Particularly more lower in the activity of blood cholinesterase in patients with very severe depression and longer course of depression. The differences were statistically significant. Based on the review of literatures, some authors suggested that the low activity of blood cholinesterase would be consistent with the hypothesis, that depression is associated with reduced cholinesterase activity in the brain. The reason for the mechanism is not clear. Whether it is a biological marker of depression, this needs further investigation.
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PMID:[The preliminary investigation of cholinesterase in depression]. 262 May 92

The measurement of plasma and erythrocyte cholinesterase activities is used to monitor absorption of anti-cholinesterase organo-phosphorus compounds. A fall in an individual's enzyme activity signifies excessive exposure if it is clearly greater than the normal intra-individual variation found in unexposed subjects. The extent of normal variation in enzyme activity as measured is dependent on both the true intra-individual biological variation and the precision of the method used. This report defines normal variation in plasma and erythrocyte cholinesterase activity using the assay developed and used routinely in our laboratory. We have also defined the relation between the precision of the assay used by a laboratory and the sensitivity with which a significant depression in successive enzyme measurements can be detected. This allows occupational physicians, who use cholinesterase measurements to monitor organo-phosphate exposure, to establish percentage depressions from their method precision data that may possibly indicate organo-phosphate uptake between successive enzyme measurements. We have calculated that, with our analytical precision, percentage drops between two successive measurements that are greater than 15 and 7.5 per cent for the plasma and erythrocyte enzymes respectively suggest significant organo-phosphorus absorption in pesticide workers.
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PMID:Intra-individual variation in plasma and erythrocyte cholinesterase activities and the monitoring of uptake of organo-phosphate pesticides. 262 38

The authors investigated in human and in experimental organophosphate intoxication the features of the toxic ECG repolarisation disturbance, the QT lengthening and its connection with cholinesterase depression. It was concluded that this pathological electrophysiological change in human intoxication does not show close correlation with the decrease of enzyme activity and cannot be influenced by atropine. The ECG alteration can be reproduced in animal experiments, it precedes the toxicologically relevant cholinesterase depression, it is pesticide dose dependent, but it cannot be induced by cholinergic or adrenergic drugs. On the basis of all this it is supposed that in organophosphate intoxication the QT lengthening reflects a direct myocardial pesticide effect and, is independent of cholinergic mediation.
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PMID:[ECG repolarization disorder (QT lengthening) in organophosphate poisoning]. 264 83


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