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

---

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

Clinical and pulmonary function changes induced by intravenous dichlorvos (2,2-dichlorvinyldimethyl phosphate) (DDVP) toxicosis, and reversibility of these changes after atropine treatment were investigated in six Friesian calves one to three months old. From one minute after dosage, all animals showed severe respiratory distress, excitation, weakness, muscle fasciculation and cholinesterase inhibition. Decrease in dynamic lung compliance and arterial oxygen tension and increase in total pulmonary resistance, viscous work of breathing and alveolar arterial oxygen gradient were highly significant (P less than 0.01). On the other hand, body secretions, heart rate, respiratory rate, tidal volume and arterial carbon dioxide tension were not significantly affected by DDVP injection. Atropine promptly and completely reversed these changes, except for muscle fasciculations, central depression and cholinesterase inhibition which disappeared progressively within 24 hours.
...
PMID:Pulmonary function changes induced by experimental dichlorvos toxicosis in calves. 373 27

Healthy camels were experimentally infected with Trypanosoma evansi and then treated with isometamidium chloride (samorin) at single intravenous doses of 0.5 or 1.0 mg/kg. Five to 10 min after the drug administration, the camels at both dosages showed lacrimation, salivation, trembling, restlessness, frequent urination and defecation, followed by diarrhea. Moreover, the camels at the higher dose showed an unsteady gait for about an hour with hindleg weakness and walking backward. The animals fell to the ground, laid on their sides, and bent their necks into an "S" shaped curve. Three hours after the drug administration all the animals stood up and remained quiet. The treatment increased the concentration of plasma ammonia and total protein. No significant change was found in the plasma bilirubin concentration. Two hours after treatment, the activity of plasma cholinesterase was significantly reduced. The enzyme activity recovered 24 h after drug administration, but was still significantly below the control value. The treatment did not produce statistically significant changes in the hemogram of the infected camels. The results suggest that the drug should not be used clinically against T evansi infection due to its low margin of safety. If the drug is to be used at all in camels, pretreatment with an anticholinergic agent might be considered.
...
PMID:Some observations on the toxicosis of isometamidium chloride (samorin) in camels. 377 85

Thirty-eight 7-week-old white leghorn chickens of two strains (high and low antibody response to sheep erythrocytes) were divided into groups for exposure to high and low levels of social stress. They were then challenged orally with a toxic dose of the organophosphate insecticide malathion (250 mg/kg body weight) and evaluated 60 min later for muscarinic signs (diarrhea, lacrimation, respiratory secretions), nicotinic signs (muscle weakness), plasma cholinesterase activity, and brain acetylcholinesterase activity. A significant correlation was shown between clinical and biochemical indices of organophosphate toxicity. The correlation between social stress and malathion toxicity was less well defined. Chickens with low antibody response preexposed to high social stress were most resistant to organophosphate toxicity.
...
PMID:Effects of social stress on the toxicity of malathion in young chickens. 381 4

A group of 16 cauliflower workers poisoned by residues of the organophosphate insecticides mevinphos and phosphamidon was followed in weekly clinics with interviews and determinations of plasma and erythrocyte cholinesterase levels. None had preexposure baseline values. Although six had initial erythrocyte cholinesterase values within the laboratory normal range, subsequent testing showed their erythrocyte activity had been significantly inhibited. While the most severe symptoms of the 16 subjects resolved after 28 days, their erythrocyte cholinesterase levels did not reach a plateau until an average of 66 days after exposure, after which most patients continued to report blurred vision, headache, weakness or anorexia. These findings support the view that the diagnostic utility of single cholinesterase levels is limited in the absence of baseline values.
...
PMID:Clinical management of field worker organophosphate poisoning. 401 66

The sensitivity of the mouse to organophosphorus-induced delayed neurotoxicity (OPIDN) has been investigated. One group of five mice received two single 1000-mg/kg po doses of tri-o-cresyl phosphate (TOCP) at a 21-day interval (on Days 1 and 21 of the study); a second group of five mice was given 225 mg/kg of TOCP daily for 270 days. A third group of five animals served as an untreated control. All animals were killed 270 days after the start of the experiment. Daily po dosing of 225 mg/kg TOCP caused a decrease in body weight gain, muscle wasting, weakness, and ataxia which progressed to severe hindlimb paralysis at termination. On the other hand, po administration of two single 1000-mg/kg doses of TOCP at a 21-day interval produced no observable adverse effects. Brain acetylcholinesterase (AChE) and neurotoxic esterase (NTE) activity were 35 and 10% of the control, respectively, in daily dosed animals while AChE and NTE in mice receiving two single 1000-mg/kg doses of TOCP were not significantly altered from the control group. Plasma butyrylcholinesterase activity was 12% of the control group in daily dosed animals. Hepatic microsomal enzyme activities of aniline hydroxylase and p-chloro-N-methylaniline demethylase and NADPH-cytochrome P-450 content in daily dosed animals were increased (141 to 161% of the control group) when compared to controls and mice receiving two single 1000-mg/kg doses of TOCP; the latter being not significantly different from each other. Degeneration of the axon and myelin of the spinal cord and sciatic fascicle were observed and were consistent with OPIDN. This study demonstrates that chronic dosing of TOCP produces OPIDN and induces hepatic microsomal enzyme activity in mice. It is concluded that while the mouse is susceptible to OPIDN, it is a less sensitive and a less appropriate test animal for studying this effect when compared to the adult hen.
...
PMID:Characterization of delayed neurotoxicity in the mouse following chronic oral administration of tri-o-cresyl phosphate. 404 9

Clinically normal Nubian goats were given the antiprotozoal drug imidocarb at single intramuscular doses of 6, 12, 18 and 24 mg/kg, and the various clinical, biochemical and pathological manifestations were recorded. At a dose of 6 mg/kg the drug produced no change in any of the parameters studied. At higher doses, the drug produced dose dependent changes which included increased heart and respiratory rates, increased defaecation, urination, depression, incoordination of movement, weakness of the hindlegs, recumbency, and finally death. Just prior to death, there was a significant decrease in the number of erythrocytes, and in packed cell volume, and haemoglobin concentration. In plasma there was an increase in the activity of aspartate transaminase, urea and creatinine concentrations and inhibition of cholinesterase activity. The main histopathological changes were associated with hepatic and renal damage. Three goats were pre-treated with atropine sulphate (1 mg/animal) and after one hour given imidocarb intramuscularly at a dose of 12 mg/kg. The changes were similar but much less severe when compared with those in animals given imidocarb alone at the same dose.
...
PMID:Some effects of imidocarb in goats. 408 55

The data obtained in mice with experimental thyrotoxic myopathy included a decrease in the median diameter of the muscle fibers by 17.1 per cent and various focal degenerative changes in less than 20 per cent of the muscle fibers; a statistically significant elevation in the activity of alpha-glycerophosphate dehydrogenase, as well as a reduction in phosphorylase activity and glycogen levels. There was also a significant diminution in the median diameter of the motor terminal plates, a decrease in cholinesterase activity and intensified collateral ramification of the distal axons. The major cause of the muscular weakness and structural changes in the skeletal muscles in thyrotoxic myopathy seems to lie in lowered cAMP concentrations and a weakened cAMP-dependent regulation of protein kinase.
...
PMID:[Pathogenesis of experimental thyrotoxic myopathy]. 624 Aug 78

Dogs exposed to topical organophosphate (fenthion) developed decreased plasma and muscle cholinesterase activities. After 2 doses were applied (1 week between doses), plasma concentrations declined 80% and muscle cholinesterase activity was reduced by 56%. Decremental responses to repetitive nerve stimulation developed after fenthion administration. Diphenhydramine, but not placebo, corrected the electrical abnormalities caused by organophosphate application, but without altering plasma or muscle cholinesterase activity. Control dogs housed in the same kennel demonstrated a slight decrease (18%) of plasma cholinesterase, which indicates that there may be potential cross contamination. Diphenydramine may be effective in treating organophosphate-induced neuromuscular weakness which is refractory to other forms of therapy.
...
PMID:Correction of organophosphate-induced neuromuscular blockade by diphenhydramine. 649 17

To investigate pathogenic mechanisms in experimental autoimmune myasthenia gravis (EAMG) and myasthenia gravis (MG), we studied the acute and chronic effects in rats of injection of rat monoclonal antibodies ( MCABs ) directed against the acetylcholine receptor (AChR). Animals were severely weak 12 h after a single injection, at which time macrophages were found invading endplate regions of muscle and cholinesterase-stained regions were separted from the underlying muscle fibers. Ultrastructural studies showed findings identical to the acute phase of EAMG: degenerating postsynaptic membranes and invasion and phagocytosis of endplate regions by macrophages. Animals receiving sublethal doses of MCAB recovered clinically by 4-5 days after injection. Recovery was accompanied by a progressive decrease in the number of macrophages associated with endplates and reapposition to the myofibers of the cholinesterase-stained regions. Animals injected once, or repeatedly over several months, remained clinically and electromyographically normal after recovery from the initial episode of weakness, but their endplate ultrastructure was highly simplified with blunted or absent synaptic folds and shallow or absent secondary synaptic clefts. These studies demonstrate that anti-AChR MCABs can induce the changes of both acute and chronic EAMG. There is good correlation between the inflammatory changes and the acute clinical disease but poor correlation between morphological and clinical parameters in the chronic syndrome. The latter observation suggests that severe ultrastructural changes, similar to those seen in chronic EAMG and MG, cannot account, at least in rats, for the clinical and electrophysiologic abnormalities of MG.
...
PMID:Induction of the morphologic changes of both acute and chronic experimental myasthenia by monoclonal antibody directed against acetylcholine receptor. 661 Feb 75

Daily dermal administration for 90 days of 0.01 to 10 mg/kg of O-ethyl O-4-nitrophenyl phenylphosphonothioate (EPN) technical grade (85%) in acetone (0.1 ml) on the unprotected back of the neck produced delayed neurotoxicity. Hens given 2.5 to 10 mg/kg daily doses also received daily doses of atropine sulfate for 5 or 6 days to protect against cholinergic acute toxicity. Severity of the clinical condition depended on the concentration of the daily dermal dose of EPN; i.e., while hens given small doses showed only ataxia, those treated with large doses progressed to paralysis and died. The most consistent histopathologic alteration was the degeneration of axons and myelin in the spinal cord which was identical to that found in positive control hens that received daily dermal doses of 5 or 10 mg/kg tri-o-cresyl phosphate (TOCP). Some of the hens treated daily with the smallest tested dose of EPN (0.001 mg/kg) which did not show clinical signs of delayed neurotoxicity showed equivocal histological changes in the spinal cord. EPN and TOCP treatments had a more profound effect on the activity of plasma butyrylcholinesterase than that of brain acetylcholinesterase (AchE). by contrast O,O,-diethyl O-4-nitrophenyl phosphorothioate (parathion) was more inhibitory to brain AChE. Negative control hens that were treated with 90 daily dermal doses of 1 mg/kg of parathion initially showed leg weakness followed by recovery. A group of hens that received the same volume of acetone (0.1 ml) daily remained normal.
...
PMID:Effect of subchronic dermal application of O-ethyl O-4-nitrophenyl phenylphosphonothioate on producing delayed neurotoxicity in hens. 668 63


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---