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)

During the last 4 years, 225 patients have been referred to the Danish Cholinesterase Research Unit following an episode of prolonged apnoea after suxamethonium. Fourteen patients (6.2%) were found to have a low serum cholinesterase activity due to an acquired deficiency (for instance, liver disease, chronic debilitating disease or carcinoma). One hundred and forty-eight patients (65.8%) had an inherited abnormal serum cholinesterase, and 105 of these patients (46.7%) were homozygous for the atypical enzyme (E1 Ea1). The mean period of apnoea in this latter group was 92 min (range: 25--240). Seventeen patients (7.6%) were heterozygous for the normal and the atypical enzyme (Eu1 Ea1), with a mean apnoea period of 25 min (range: 7--60 min). Twelve patients were found to be heterozygous for the atypical and the silent gene (E(a)1 E(s)1). The mean period of apnoea was 126 min (range: 45--210 min). Fourteen patients had other rare genotypes. The longest mean period of apnoea (170 min, range: 70--330) was found in patients homozygous for the silent gene (Es1 Es1). The silent gene and the fluoride-resistant gene were found in 8.9% and 2.7% of the patients, respectively. In 63 patients (28.1%) both the type and quantity of serum cholinesterase were normal. In 34 of these patients (15.2%), the prolonged apnoea was due to other causes; for example, suxamethonium overdose, hyperventilation and central as well as peripheral respiratory depression. However, in the other 29 patients (12.9%), the reason for the prolonged apnoea could not be established. The possibility therefore exists that these cases represent unknown genotypes.
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PMID:Prolonged apnoea after suxamethonium: an analysis of the first 225 cases reported to the Danish Cholinesterase Research Unit. 72 55

Increasingly widespread application of organophosphate pesticies has underscored the importance of studying their effects on human behavior. Clinical reports and laboratory investigations have generally supported the assumption that neurobehavioral manifestations of organophosphate toxicity are attributable to accumulation of acetylcholine at central and peripheral synapses as a result of cholinesterase inhibition. Despite methodologic shortcomings in many of the published studies, investigators generally agree on the presence of several behavioral sequelae of organophosphate poisoning: (a) impaired vigilance and reduced concentration, (b) slowing of information processing and psychomotor speed, (c) memory deficit, (d) linguistic disturbance, (e) depression, and (f) anxiety and irritability. The few studies of asymptomatic workers at risk for repeated exposure to organophosphate pesticides have produced only equivocal findings concerning the presence of less severe or latent forms of these behavioral abnormalities.
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PMID:Behavioral effects of organophosphate in man. 78 76

A field trial was set up to test the prophylactic properties of the organophosphorous drug metrifonate (Bilarcil Bayer AG). Subjects were rural African children living in an area of Rhodesia where Schistosoma haematobium and S. mansoni are highly endemic. The trial was conducted in three stages, a preliminary period of therapy followed by two six-month periods of prophylaxis. Parasitological and haematological tests were carried out monthly and major assessments (including clinical examinations) were carried out prior to the start of the trial and at the end of each of the three stages. Drug was given to the appropriate groups at a dose rate of 7-5 mg/kg once per fortnight for three doses during the therapy stage and four-weekly during the prophylaxis stage. Results with S. haematobium were very good. A 60% cure-rate was observed six weeks aection was obtained in those children continuing to receive the drug as a prophylactic, even during the season of highest transmission; intensities of infection in those who became infected were very low. Infection rates in the treated but unprotected group rose steadily from 40% at week 11 to 95% at week 70. There was a sigificant effect upon the intensity of S. mansoni infections only when pre- and post-trial data were compared. Apart from the anticipated (and previously reported) depression of plasma cholinesterase values no side effects were recorded. Drug tolerance and acceptibility were very high. It is likely that the costs of a year's protection against S. Haematobium using metrifonate will be significantly lower than protection by molluscicidal techniques or single courses of treatment with established drugs.
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PMID:Field trial of metrifonate in the treatment and prevention of schistosomiasis infection in man. 84 20

Clinical signs, pathologic changes and biochemical changes occurred in cattle with natural and experimental triaryl phosphate poisoning. Natural poisoning was caused by triaryl phosphates escaping from a gas pipeline compressor station. The clinical signs were posterior motor paralysis, dyspnea, diarrhea and agalactia. Experimental doses of 1/2-1 gm/kg body weight of these organophosphate compounds caused depression of cholinesterase and axonal degeneration in the spinal cord.
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PMID:Triaryl phosphate poisoning in cattle. 85 97

To acquire information regarding the potential hazard of pesticide-impregnated collars to dogs, 13 male Beagles were allotted to 2 groups; 8 of the dogs were fitted wtih propoxur-impregnated tick and flea collars and the other 5 were fitted with placebo collars. All dogs wore their collars for 42 consecutive days. The dogs wearing test collars had significant (P less than 0.01) depression of erythrocyte and plasma cholinesterase activities at day 1 after collar application; however, the enzyme activity values returned to the preexposure range within 3 days. Miosis, with decreased pupillary response, was noticed during the 1st week of exposure. Irritation of the skin of the neck was mild and transient in both the test and control groups from the 2nd week onward.
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PMID:Evaluation of a carbamate-impregnated flea and tick collar for dogs. 89 10

The effects of oral prednisone on plasma and red blood cell cholinesterases have been studied in human volunteers. While the activity of plasma pseudocholinesterase is depressed by glucocorticoid administration, the activity of red blood cell true cholinesterase is not affected. Cortisol administration to rats, intraperitoneal or subcutaneous, inhibited liver pseudocholinesterase activity, indicating a possible depression of the enzyme protein synthesis.
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PMID:Effect of glucocorticoids on liver and blood cholinesterases. 92 92

In anesthetized cats, whose peripheral muscarinic-cholinorecptors are blocked by m-cholinolytics (benzilyl choline) failing to penetrate into the brain, the cholinesterases reactivator diethyxime debars the centrally caused fall of the arterial pressure produced by armine, an inhibitor of cholinesterases readily gaining access into the brain. Diethyxime is also capable of abolishing the depression of the phrenic nerve action potentials produced by armine. Dipyroxime-a quaternary diethyxime analogue and also a quaternary cholinesterase reactivator fails to produce such an effect.
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PMID:[Central action of a new cholinesterase reactivator, diethyxime]. 92 73

Azinphos-methyl was evaluated for its subchronic inhalation toxicity. The exposure of rats to concentrations of 0.195, 1.24, and 4.72 mg/m3, respectively, for 12 weeks, 6 hrs daily, 5 times weekly, resulted in effects only in those animals which inhaled aerosols of the highest concentration. This group showed a significant depression of the cholinesterase activity in plasma and erythrocytes. The males of this group had a lower body weight gain. The results are in agreement with the established maximum allowable concentration of 0.2 mg/m3.
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PMID:Subchronic inhalation toxicity of azinphos-methyl in rats. 94 16

Pancuronium causes a powerful and highly selective inhibition of human serum cholinesterase in vitro. The inhibition was studied in serum from 14 individuals of both sexes (5-60 years of age) with normal reactions to suxamethonium. Pancuronium, in a concentration of 2.3 x 10(-7) M, caused a 50% inhibition of the enzymatic hydrolysis of acetylcholine, when this substrate was present in a concentration of 10 x 10(-3) M. The same I50 value was also found for a commercial preparation of human serum cholinesterase. The inhibition was reversible and competitive in type. Pancuronium inhibition of the acetylcholinesterase in human red blood cells and from the electric eel was more than one thousand times weaker. Thus pancuronium is one of the most selective inhibitors of serum cholinesterase described so far. The in vivo activity of the serum cholinesterase in four patients receiving pancuronium 0.1 mg/kg decreased, during the first 3 min, by 60-80%, from the pre-induction value. After this a slow recovery occurred with 40% depression remaining at 45 min after the injection. The tachycardia produced by pancuronium may be related to this selective inhibition of serum cholinesterase. It is suggested that relaxants which selectively inhibit serum cholinesterase also selectively block the cardiac muscarinic receptors.
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PMID:The inhibition of cholinesterases by pancuronium. 119 83

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


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