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:3.1.1.7 (acetylcholinesterase)
28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism of interaction between chlorpyrifos, an organophosphate insecticide, and methyl mercury was assessed utilizing the amphipod, Hyalella azteca. Previous studies have demonstrated that chlorpyrifos and methyl mercury interact additively with survival as the endpoint. In addition, exposure to chlorpyrifos and methyl mercury increased the accumulation and decreased the elimination of methyl mercury. To further examine the mechanism responsible for these interactions, the in vivo and in vitro inhibition of acetylcholinesterase enzyme activity was assessed following exposure to methyl mercury and chlorpyrifos. In vivo, methyl mercury antagonized the effects of chlorpyrifos on acetylcholinesterase inhibition. Additional studies demonstrated that methyl mercury did not affect the in vitro bioactivation of chlorpyrifos or the subsequent inhibition of acetylcholinesterase enzyme activity. Chemical-chemical interactions were examined utilizing chromatographic techniques and suggested the formation of a chlorpyrifos-methyl mercury complex. The formation of this complex may result in increased accumulation of methyl mercury, apparent additive toxicity, and protection against chlorpyrifos-mediated acetylcholinesterase inhibition.
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PMID:Interactions of chlorpyrifos and methyl mercury: a mechanistic approach to assess chemical mixtures. 1146 Jun 76

Recent studies have reported on the toxicity and related oxidative stress of selenium and mercury. The present study compares the effects of Se as sodium selenite (Na2SeO3) and Hg as mercuric chloride (HgCl2) separately and in combination. Rats received repeated oral doses of Se (0.5 micromol/ml), Hg (0.5 micromol/ml), or Se in combination with Hg (0.5 micromol/ml of each) for 5 consecutive days. Rat serum, brain and liver samples were collected for biochemical assays. The following biochemical alterations occurred in response to Hg treatment: protein content (brain and liver), acetylcholinesterase (AChE) (brain and serum), acid and alkaline (AcP and AlP) phosphatases (plasma and liver) and glutathione S-transferase (GST) (plasma and liver) activities were significantly (P<0.05) decreased, while lactate dehydrogenase (LDH) (plasma, brain and liver), aspartate and alanine aminotransferase (AST, ALT) (serum and liver) activities were significantly increased. Thiobarbituric acid reactive substances (TBARS) was significantly increased in brain and liver. Effect of Se alone included decreased AcP, AlP and GST (serum and liver) activities. However, LDH (serum, brain and liver) and AST (liver) and TBARS (brain and liver) increased. Selenium in combination with Hg partially or totally alleviated the toxic effects of Hg on different studied enzymes. It is concluded that Se could be able to antagonize the toxic effects of mercury.
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PMID:Effects of selenium and mercury on the enzymatic activities and lipid peroxidation in brain, liver, and blood of rats. 1149 25

The measurement of contaminant tissue concentrations or exposure-related effects in biota has been used extensively to monitor pollution and environmental health. Terrestrial vertebrates have historically been an important group of species in such evaluations, not only because many are excellent sentinels of environmental contamination, but also because they are valued natural resources in their own right that may be adversely affected by toxicant exposure. Selection of appropriate vertebrates for biomonitoring studies frequently relies on expert opinion, although a few rigorous schemes are in use for predicting vulnerability of birds to the adverse effects of petroleum crude oil. A Utility Index that ranks terrestrial vertebrate species as potential sentinels of contaminants in a region, and a Vulnerability Index that assesses the threat of specific groups of contaminants to these species, have been developed to assist decision makers in risk assessments of persistent organic pollutants, cholinesterase-inhibiting pesticides, petroleum crude oil, mercury, and lead shot. Twenty-five terrestrial vertebrate species commonly found in Atlantic Coast estuarine habitat (Rattner et al. 2001a) were ranked for their utility as biomonitors of contamination and their vulnerability to pollutants in this region. No single species, taxa, or class of vertebrates was found to be an ideal sentinel for all groups of contaminants. Although birds have overwhelmingly been used to monitor contaminants compared to other terrestrial vertebrate classes, the nonmigratory nature and dietary habits of the snapping turtle and mink consistently resulted in ranking these species as excellent sentinels as well. Vulnerability of Atlantic Coast populations of these species varied considerably among groups of contaminants. Usually a particular species was found to be at high risk to only one or two groups of contaminants, although a noteworthy exception is the bald eagle, which is highly vulnerable to all five of the contaminant groups examined. This index could be further enhanced by generation of additional comparative toxicity data to facilitate interspecific extrapolations. The Utility and Vulnerability Indices have application to many types of habitats in addition to estuaries and are of value to natural resource and risk managers that routinely conduct local, regional, or national environmental quality assessments.
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PMID:Ranking terrestrial vertebrate species for utility in biomonitoring and vulnerability to environmental contaminants. 1244 4

Signal transduction by xenobiotics in fish has recently gained much attention. The better known transduction mechanisms are those elicited by organochlorines, organophosphates, carbamates and heavy metals. Organochlorines specifically bind to the membrane bound ouabain sensitive Na+-K+-ATPase affecting neural transmission while the organophosphates and carbamates bind specifically to the membrane bound enzyme acetylcholinesterase again affecting neural transmission. Since the nervous system is one of the important integrative and interactive physiological systems in animals, hypofunction of the nervous system leads to secondary effects in the endocrine system including thyroidal, gonadal, interrenal, pituitary and hypothalamic functions. Even low levels of xenobiotics are efficient enough to bring about remarkable changes in the functional physiology of the non target animals. Heavy metals such as cadmium or mercury belonging to the same group II B in the periodic table probably have a similar mechanism of action. Avidity of these metals to SH-radicals allow them to bind indiscriminately to SH groups in proteins. One pathway of interaction by inorganic mercury with the membrane bound ouabain sensitive Na+-K+-ATPase has been clearly established in fish liver and ovary. Binding of inorganic mercury to the membrane bound enzyme is through sulfhydryl group which inactivates the sodium pump leading to accumulation of the cation in the cytosol. The inorganic mercury is next conjugated by the cytosolar nucleophile, glutathione, and is transported to the nucleus where dissociation occurs and the free metal binds to the metal regulatory element to initiate gene expression. The inducible proteins are 3beta-hydroxysteroid dehydrogenase in the oocyte and metallothionein and C-reactive protein in the liver. The present review deals with the role of xenobiotic as a stress factor.
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PMID:Signal transduction by xenobiotics in fish. 1255 5

The environmental impact and recovery associated with the long and uninterrupted disposal of large volumes of moderately contaminated dredged material from the port of Rotterdam was studied at nearby dumping sites in the North Sea. Observations were made on sediment contamination, ecotoxicity, biomarker responses and benthic community changes shortly after dumping at the 'North' site had ceased and at the start of disposal at the new dumping site 'Northwest'. During the period of dumping, very few benthic invertebrates were found at the North site. Concentrations of cadmium, mercury, polychlorinated biphenyls (PCBs), polyaromatic hydrocarbons (PAHs) and tributyltin (TBT) in the fine sediment fraction (<63 microm) from this site were 2-3 times higher than at the reference site. In four different bioassays with marine invertebrates the sediments showed no acute toxic effects. In tissue (pyloric caeca) of resident starfish Asterias rubens, residual levels of mercury, zinc, PCBs and dioxin-like activity were never more than twice those at the reference site. Four different biomarkers (DNA integrity, cytochrome P450 content, benzo[a]pyrene hydroxylase activity and acetylcholinesterase inhibition) were used on the starfish tissues, but no significant differences were found between North and the reference site. Minor pathological effects were observed in resident dab Limanda limanda. One year after dumping had ceased at the North site, a significant increase in the species richness and abundance of benthic invertebrates and a concomitant decrease in the fine sediment fraction of the seabed were observed. After 8.2 million m3 of moderately contaminated dredged material had been dumped at the new dumping site Northwest, the species richness and abundance of benthic invertebrates declined over an area extending about 1-2 km eastwards. This correlated with a shift in sediment texture from sand to silt. The contamination of the fine sediment fraction at the Northwest location doubled. It is concluded that marine benthic resources at and around the dumping sites have been adversely affected by physical disturbance (burial, smothering). However, no causal link could be established with sediment-associated contaminants from the dredged spoils.
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PMID:Environmental impact and recovery at two dumping sites for dredged material in the North Sea. 1268 79

Fathead minnows (Pimephales promelas) were exposed to mercury (1.69, 6.79, and 13. 57 microg/L HgCl(2), 10 days exposure), and afterward their foraging ability was tested in a vegetated habitat for 7 days. Among the foraging metrics used were foraging efficiency, capture speed, and the ability to learn and retain information regarding habitat characteristics. In addition to behavioral tests, muscle tissue acetylcholinesterase activity and brain levels of several neurotransmitters were investigated. Comparisons with control fish and fish from the two highest exposure groups revealed consistent performance deficits in foraging efficiency and capture speed. However, no treatment effects on learning were detected, nor were differences in neurotransmitter levels detected. In determining the underlying proximate cause of the foraging deficits, it is believed that the greater pause time exhibited by treatment fish while foraging was the main cause of treatment differences. In the future, behavioral studies will continue to allow toxicity testing of environmentally relevant variables such as those used by behavioral ecologists.
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PMID:The effect of mercury on the feeding behavior of fathead minnows (Pimephales promelas). 1274 68

Mercury contamination of fish is widespread in North America and has resulted in the establishment of fish consumption advisories to protect human health. However, the effects of mercury exposure to fish have seldom been investigated. We examined the effects of dietary mercury exposure at environmental levels in a common forage species, golden shiner (Notemigonus crysoleucas). Fish were fed either an unaltered diet (12 ng/g wet wt methylmercury [MeHg] as Hg), a low-Hg diet (455 ng/g Hg), or a high-Hg diet (959 ng/g Hg). After 90 d mean fish whole-body total Hg concentrations were 41, 230, and 518 ng/g wet wt, respectively, which were within the range of concentrations found in this species in northern U.S. lakes. There were no mortalities or differences in growth rate among groups. Groups of fish from each treatment were exposed to a model avian predator and their behavioral response videotaped for analysis. Brain acetylcholinesterase (AChE) activity was determined in fish after behavioral testing. Fish fed the high-Hg diet had significantly greater shoal vertical dispersal following predator exposure, took longer to return to pre-exposure activity level, and had greater shoal area after return to pre-exposure activity than did the other treatments, all of which would increase vulnerability of the fish to predation. There were no differences in brain AChE among treatments. We conclude that mercury exposure at levels currently occurring in northern United States lakes alters fish predator-avoidance behavior in a manner that may increase vulnerability to predation. This finding has significant implications for food chain transfer of Hg and Hg exposure of fish predators.
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PMID:Mercury effects on predator avoidance behavior of a forage fish, golden shiner (Notemigonus crysoleucas). 1283 81

The aim of the present investigation was to evaluate the effect of a subchronic treatment (30 days/30 doses) with subcutaneous injections (0.1 mg/kg) of HgCl2 on NTPDase (E.C. 3.6.1.5), 5'-nucleotidase (E.C 3.1.3.5) and acetylcholinesterase (AChE, E.C. 3.1.1.7) activities in brain from adult rats. NTPDase and 5'-nucleotidase were measured in cortical synaptosomal fraction and AChE was measured in the homogenate of cerebral cortex and hippocampus. After the subchronic treatment (30 days), NTPDase activity was enhanced approximately 35% (p < 0.05) with ATP and ADP as substrates and no difference was observed in 5'-nucleotidase activity (AMP hydrolysis). In addition, AChE activity was enhanced in the cerebral cortex (22%, p < 0.05) and hippocampus (26%, p < 0.05) after the subchronic treatment. Mercury deposited in brain was measured by cold vapor (atomic absorption spectrometry) and no difference between the control and the subchronically treated group was observed. Here we showed for the first time that exposure to low levels of Hg2+, which resembles occupational exposure to low levels of mercury, caused a marked increase in NTPDase and AChE activities. The relationship of these alterations with the neurotoxicity of inorganic mercury deserves further studies.
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PMID:Effect of subchronic treatment with mercury chloride on NTPDase, 5'-nucleotidase and acetylcholinesterase from cerebral cortex of rats. 1513 88

Carp (Cyprinus carpio) and barbel (Barbus graellsii) were collected from five sites along the Ebro River. The study was designed to assess levels of persistent organic pollutants and metals bioaccumulated by fish, and some biochemical responses (cytochrome P450 system, phase II activities, and metallothioneins) against those pollutants. The highest levels of PCBs and DDTs were detected in carp from industrialised areas, which also showed high levels of mercury and cadmium in the liver, and high levels of nonylphenol in bile. Significant alterations in some biochemical markers were observed and associated to combined exposure to pollutants. The activity 7-ethoxyresorufin O-deethylase ranged from 69 pmol/min/mg protein in carp from the reference site to 415 pmol/min/mg protein in those from polluted sites. Carp from the Ebro Delta, an agricultural area, had depressed acetylcholinesterase in muscle tissue. Metallothionein concentrations were positively correlated with copper residues, but no significant differences among sampling points were observed.
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PMID:The combined use of chemical and biochemical markers to assess water quality along the Ebro River. 1604 Jan 74

Only a few drugs can induce drooling (sialorrhea or hypersalivation) to a clinically significant degree. When significant drooling occurs, however, it can pose a vexing management problem. Drooling is either caused by an increase in saliva flow that cannot be compensated for by swallowing, or by impaired swallowing that cannot handle normal or even reduced amounts of saliva. Major medication groups that are clearly associated with drooling are antipsychotics, particularly clozapine, and direct and indirect cholinergic agonists that are used to treat dementia of the Alzheimer type and myasthenia gravis. Drooling is also caused by certain heavy metal toxins (mercury and thallium); from exposure to irreversible acetylcholinesterase inhibitors (insecticides and nerve agents); and by a handful of other drugs (e.g., yohimbine, mucosa-irritating antibiotics). The treatment of medication-induced drooling is often only symptomatic and attempts to decrease saliva to amounts that can be swallowed (to prevent "pool and drool"). Most pharmacological approaches reduce cholinergic tone, either systemically (e.g., atropine-related oral anticholinergics) or more locally (e.g., sublingual ipratropium spray); or increase adrenergic tone (e.g., clonidine patch). Recently, botulinum injections into the parotid gland have been used successfully to treat refractory cases.
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PMID:Drug-induced sialorrhea. 1611 Mar 48


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