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:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to assess the influence of renal function on the pharmacokinetics, pharmacodynamics, safety, and tolerability of the acetylcholinesterase inhibitor metrifonate. Four groups of six age- and gender-matched subjects with varying degrees of renal function (creatinine clearances more than 90, 60-90, 30-60, and less than 30 mL/min/ 1.73 m2, respectively) were administered a single 50-mg oral dose of metrifonate. Blood and urine samples were collected for 24 hours and concentrations of metrifonate and its metabolites dichlorvos, dichloroacetic acid, and M3 were determined. Inhibition of acetylcholinesterase activity in erythrocytes and butyrylcholinesterase in plasma were also measured. Metrifonate was well tolerated in all treatment groups. The urinary excretion of metrifonate and dichlorvos decreased with decreasing renal function but accounted for less than 2% of the elimination. There were no statistically significant differences in primary pharmacokinetic parameters--Cmax, t(max), area under the concentration-time curve (AUC), and t1/2--of metrifonate and dichlorvos among the different groups. The excretion of dichloroacetic acid and M3 was not influenced by renal impairment. Acetylcholinesterase was not inhibited, whereas butyrylcholinesterase was inhibited markedly but independently of renal function. No metrifonate dose adjustments are needed when treating subjects with renal impairment.
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PMID:Pharmacokinetics and pharmacodynamics of the acetylcholinesterase inhibitor metrifonate in patients with renal impairment. 1036 43

The urinary excretion rates of dimethyl-phosphate, -phosphorothioate and -phosphorodithioate were studied in six persons of whom four had ingested a concentrated solution of malathion and two of thiometon. The concentration decrease of single and total dimethylphosphorus metabolites was biphased, with a fast initial rate and a slow later rate. The excretion rate of total metabolites in the faster phase depended on the initial concentration in urine. At concentrations higher than 100 nmol/mg creatinine, the excretion half-times ranged from 7.5 to 15.4 h and at concentrations between 52 and 95 nmol/mg creatinine from 34.7 to 55.4 h. Non-metabolized malathion was detected only in one urine sample collected from one person immediately after hospitalization. Two persons poisoned with malathion were taken blood serum samples for the analysis of the parent pesticide and its metabolites on a daily basis after hospitalization. The parent pesticide was detectable in the serum only one day after the poisoning. The concentration of total malathion dimethylphosphorus metabolites in serum decreased very quickly within 1.5 days after hospitalization. The total metabolite elimination half-times were 4.1 and 4.7 h in the initial phase, and 53.3 and 69.3 days in the later slower elimination phase. There was no correlation between maximum concentrations of total metabolites measured in serum and/or urine on the day of admission to hospital and the initial depression of serum cholinesterase (BChE, EC 3.1.1.8) and erythrocyte acetylcholinesterase (AChE, EC 3.1.1.7).
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PMID:Dimethylphosphorus metabolites in serum and urine of persons poisoned by malathion or thiometon. 1042 86

The purpose of this study was to investigate the effect of melatonin, at pharmacological doses, on serum lipids of rats fed with a hypercholesterolemic diet. Therefore, different groups of animals were fed with either the regular Sanders Chow diet or a diet enriched in cholesterol. Moreover, animals were treated with or without melatonin in the drinking water for 3 months. We show that melatonin treatment did not affect the levels of cholesterol or triglycerides in rats fed with a regular diet. However, the increase in total cholesterol and low-density lipoprotein (LDL)-cholesterol induced by a cholesterol-enriched diet was reduced significantly by melatonin administration. On the other hand, melatonin administration prevented the decrease in high-density lipoprotein (HDL)-cholesterol induced by the same diet. No differences in the levels of very low-density lipoprotein (VLDL)-cholesterol and triglycerides were found. We also found that melatonin administration slightly decreased serum uric, bilirubin and increased serum glucose levels. Other biochemical parameters, including total proteins, creatinine, urea, phosphorus, calcium, glutamic oxalacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), gamma-glutamyltranspeptidase (gamma-GT), acetyl cholinesterase (AcCho), and alkaline phosphatase (ALP) were not modified by melatonin treatment. Finally, lipid peroxidation (LPO) was studied in membranes of liver, brain, spleen, and heart as an index of membrane oxidative damage. Results show that hypercholesterolemic diet did not modify the LPO status in any of the tissues studied. However, chronic melatonin administration significantly decreased LPO. Results confirm that melatonin participates in the regulation of cholesterol metabolism and in the prevention of oxidative damage to membranes.
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PMID:Serum cholesterol and lipid peroxidation are decreased by melatonin in diet-induced hypercholesterolemic rats. 1073 1

The influence of sodium fluoride on the course of repair process in the mechanically injured rat bone was studied. Thirty six male Wistar rats aged 5 months, weighing 460-540 g were investigated. The animals lived under standard conditions and were fed ad libidum with the standard LSM food including 0.7 mg/kg of fluorine on the average. The animals randomly divided into 3 groups that comprised study and control groups, 6 rats each. The rats in the first group were given water with 20 mg (1.05 mmol) of sodium fluoride per kg of body weight for 24 h over a period of 2 weeks--group Ia. In the second group--IIa--animals were given water with sodium fluoride at a dose of 1.5 mmol/kg b.w./24 h for a period of 4 weeks. In the third group--IIIa--the animals were given sodium fluoride in a dose of 1.5 mmol/kg b.w./24 h for a period of 6 weeks. The rats from the control groups I, II and III were given water without sodium fluoride for the period of 2, 4 and 6 weeks, respectively. At the beginning of the experiment a hole was drilled in both femoral bones in rat under barbiturate anaesthesia. According to the protocol the rats underwent ether euthanasia after 2, 4 and 6 weeks after surgery and the following samples were collected: blood from the heart for biochemical studies and both femoral bones for biochemical and histological studies. The following parameters were evaluated in blood serum: fluorine, calcium, magnesium contents, serum concentrations of urea, creatinine, bilirubin and activity levels of enzymes: aspartate aminotransferase, alanine aminotransferase, cholinesterase, base phosphatase. Fluorine, calcium magnesium and zinc contents were estimated in bone samples. The concentration of fluorine ions in animal serum after 2, 4 and 6 weeks of experiment increased significantly as compared with the corresponding controls. The highest fluorine concentrations were observed in serum of rats supplemented with NaF for 6 weeks. The fluorine concentrations in the bone tissue and fresh and dried granulation tissues in all studied groups also revealed statistically significant increase as compared to the controls. The rats fed with sodium fluoride for the period of 6 weeks revealed statistically significant increase of serum magnesium concentration as compared to the remaining study groups. Bone magnesium concentrations in animals fed with NaF for the period of 2 and 6 weeks were higher as compared to the corresponding control groups, with the highest differences observed after 6 weeks of experiment. Animals fed with sodium fluoride for the period of 6 weeks revealed increased serum calcium concentrations as compared to the study groups after 2 and 4 weeks of experiment. Similar results were achieved in bone tissue samples (Fig. 1 and 2, Tab. 1-6). Basing on the achieved results in biochemical studies and histological pictures it should be assumed that laboratory animals fed with sodium fluoride in doses recognised as non-toxic reveal intensified healing process within mechanically injured bones. The use of sodium fluoride led to accelerated chondrogenesis process in the area of insufficiently perfused bone, osteogenesis including temporary callus formation and mineralization of the new bone, as well as remodelling into mature lamellar bone. The greatest differences in the repair dynamics for both groups occurred between the second and fourth week of experiment. These results could be the base of clinical studies on application of the sodium fluoride in the acceleration of fracture healing.
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PMID:[Evaluation of the repair process in mechanically injured rat bone stimulated by sodium fluoride with non-toxic doses]. 1090 90

Liver transplantation is the only therapeutic option for patients with end-stage liver disease. Nitric oxide, a free radical produced from L-arginine, a potent vasodilator, also inhibits platelet adhesion and aggregation, reduces adhesion of leukocytes to the endothelium and suppresses proliferation of vascular smooth muscle cells. The inducible form of the nitric oxide synthase may generate large quantities of nitric oxide, and may be induced by the action of cytokines and lipopolysaccharides. Nitric oxide can be released from the hepatic vascular endothelium, platelets and Kupffer cells as a response to ischemia-reperfusion injury and circulatory shock. We analyzed the relationships between the levels of nitric oxide, hepatic enzymes and other clinical parameters (glucose, total proteins, total bilirubin, creatinine, albumin) obtained in serum samples before liver transplantation and every 48 h till day 15 in 15 patients aged 40 +/- 13 years. Aspartate aminotransferase and alanine aminotransferase levels changed from high at the beginning, to almost normal at the end of the study, cholinesterase levels remained decreased throughout the study and nitric oxide remained high, never reaching normal values.
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PMID:Nitric oxide in liver transplantation. 1175 5

To examine the effects of occupational and environmental neurotoxicants on vestibular, cerebellar and spinocerebellar functions, the following three groups of subjects were examined, using a computerized posturography with sway frequency analysis: (1) 49 male chemical factory workers exposed to lead stearate, aged 27-63 (mean 43) years, with concurrent blood lead concentrations (BPbs) of 11-113 (mean 48) microg/100 g and past mean BPbs of 7-52 (mean 24) microg/100 g; (2) 29 male sandal, shoe and leather factory workers, aged 35-73 (mean 51) years, with urinary 2,5-hexanedione (HD) concentrations of 0.41-3.06 (mean 1.20) mg/g creatinine; and (3) 9 females, aged 19-58 (mean 29) years, who were exposed to sarin accidentally 6-8 months before the study (Tokyo Subway Sarin Poisoning, March 20,1995) and showed plasma cholinesterase (ChE) activities of 13-95 (mean 68) IU/l on the day of poisoning. The pattern of posturographic changes in lead workers suggested that the vestibulocerebellum (lower vermis), anterior cerebellar lobe and spinocerebellar afferent pathway were asymptomatically affected; the vestibulocerebellar change reflected concurrent lead absorption and the anterior cerebellar one reflected past absorption. Similarly, vestibulocerebellar and spinocerebellar functions were affected by n-hexane in solvent workers; the effect on the vestibulocerebellar function was probably inhibited by xylene. Also, the chronic (long-term) effect on the vestibulocerebellar function persisted in acute sarin poisoning. It is thus suggested that the vesitibulocerebellar function is most sensitive to all the three chemicals examined. It appears that the computerized posturography with frequency analysis is a useful technique for assessment of vestibular, cerebellar and spinocerebellar effects in occupational and environmental health.
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PMID:Computerized posturography with sway frequency analysis: application in occupational and environmental health. 1192 10

A 73-year-old man consumed a decoction of the medicinal herb Erycibe henri Prain ("Ting Kung Teng"), as recommended in traditional Chinese medicine for arthritis. Shortly, he developed a cholinergic syndrome that included dizziness, diaphoresis, chills, lacrimation, salivation, rhinorrhea, nausea, and vomiting. He was also hypothermic and hypotensive. Notable laboratory values included a normal serum cholinesterase and transiently elevated blood urea nitrogen, creatinine, and glucose. There is no previous report on the toxicity due to this herb in the literature. Active constituents of the herb include a number of tropane alkaloids, one of which possesses cholinergic rather than anticholinergic activities. A study conducted on mice, with a related herb, has demonstrated renal, hepatic, and erythrocyte toxicity.
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PMID:Medicinal herb Erycibe henri Prain ("Ting Kung Teng") resulting in acute cholinergic syndrome. 1212 92

Organophosphates (OPs) are readily absorbed through the skin and biological monitoring is an essential component of any comprehensive assessment of exposure. This paper presents a summary of our experience in a wide range of occupational studies. Additionally, we have conducted studies of non-occupational exposure and human volunteer studies looking at the kinetics of chlorpyrifos, propetamphos, diazinon and malathion. In non-occupationally exposed people, 95% of urinary alkyl phosphates do not exceed 72 micromol/mol creatinine. In occupationally exposed people, the corresponding 95th percentile of total urinary alkyl phosphates is 122 micromol/mol creatinine. In volunteer studies with 1 mg oral doses of chlorpyifos, diazinon and propetamphos the mean peak values were 160, 750 and 404 micromol/mol creatinine, respectively, and were not associated with any reduction in blood cholinesterase activity. The levels of OP metabolites seen in urine from workers potentially exposed to OPs are generally low and unlikely to cause significant reduction in blood cholinesterase activity.
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PMID:Biological monitoring of exposure to organophosphate pesticides. 1219 66

Several studies have reported the occurrence of sensory neuropathy with exposure to chlorpyrifos and other organophosphorus insecticides, at levels not associated with overt toxicity. We evaluated 113 chemical workers, including 53 of 66 (80%) eligible chlorpyrifos workers and 60 of 74 (81%) randomly selected referent workers, to identify evidence of sensory neuropathy or subclinical neuropathy. Compared to referents, chlorpyrifos subjects had significantly longer duration of work in chlorpyrifos-exposed areas (9.72 vs. 0.01 years; P < 0.0001), greater cumulative chlorpyrifos exposure (64.16 vs. 0.69 mg/m(3). day; P < 0.0001), higher urine 3,5,6-trichloro-2-pyridinol (TCP) excretion (108.6 vs. 4.3 microg/g creatinine; P < 0.0001), and lower plasma butyrylcholinesterase (BuChE) activity (7281 vs. 8176 mU/ml; P = 0.003). Despite exposures among chlorpyrifos subjects to levels at which well-described physiological effects on B-esterases exist, the frequency of symptoms or signs of neuropathy did not differ significantly between groups, and the only 2 subjects fulfilling criteria for confirmed neuropathy were both in the referent group. Mean nerve conduction study results were comparable to established control values and did not differ significantly between groups. We found no evidence of sensory neuropathy or isolated peripheral abnormalities among subjects with long-term chlorpyrifos exposure at levels known to be associated with the manufacturing process.
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PMID:Absence of sensory neuropathy among workers with occupational exposure to chlorpyrifos. 1511 71

Nephrotic syndrome (NS) remains a serious clinical setting characterized by marked proteinuria, hypoproteinemia and hypercholesterolemia, usually accompanied by the presence of oedemas. It could be presumed, that the newly discovered hormone leptin plays an important role in the complex metabolic processes occurring in patients with NS, in which apart from the changes in the hydratation, and the protein and lipid spectre profile changes, the alteration of the metabolism of glycides elicited by the treatment with corticosteroids (CS) is often observed. The aim of the study was to investigate the plasma levels of leptin and its plasma soluble receptor (sLe-R) before and after the treatment with CS and to evaluate their relationship with albuminemia and/or proteinuria. The study group consisted of 15 men and 15 women (mean age 49 +/- 13.7 years) with newly diagnosed NS, verified by renal biopsy, in which subsequently CS treatment was started. Before the treatment (period 1) and further one month (period 2) and six months (period 3) after the start of the treatment the following parameters were measured: body mass index (BMI), serum levels of creatinine, albumin, cholesterol, triglyceride, cholinesterase, proteinuria/24 hour and plasma levels of leptin and sLe-R. In comparison to the relatively high values of BMI in the period 1 a decrease of BMI towards the physiologic range was observed during the treatment periods. Statistically significant changes were also observed in proteinuria (decrease) and in serum cholesterol and albumin levels of whereas in other biochemical parameters, including plasma leptin and sLe-R levels, statistically significant changes were not found. A trend to negative correlation with borderline statistical significance could be observed between leptin and sLe-R. The results of our relatively unique study on leptin--dealing with long-term follow-up of the patients with NS suggest that regardless prominent metabolic alterations present in NS the plasma levels of leptin and sLe-R remain relatively stable, and that of regulation of leptin in this setting is probably complex and multifactorial.
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PMID:[Leptin in patients wit nephrotic syndrome]. 1522 34


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