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)

Biochemical indices were investigated for their potential use as variables of sublethal toxicity in Daphnia (cholinesterase) and Chironomus (cholinesterase and biotransformation enzymes). Parathion, dichlorvos, and aldicarb caused dose-related inhibition of cholinesterase (ChE) in 24-h bioassays with both species. Ratios of Daphnia and Chironomus ChE IC50 values to corresponding immotility EC50 values derived from the same experiment covered the range 0.26 to 1.2. Estimates of the ChE inhibition caused by the immotility EC50 were in the range 53-99% below control activity. ChE IC50 values of dichlorvos, parathion, and aldicarb were 0.17, 0.61, and 95 microg/liter in Daphnia and 6.2, 2.9, and 27 microg/liter in Chironomus, respectively. Cytochrome P450-dependent monooxygenase activities (ethoxyresorufin-O-deethylase, methoxyresorufin-O-deethylase, and ethoxycoumarin-O-deethylase) were detectable in Chironomus but not in Daphnia. Chironomus monooxygenase activities were significantly inhibited to about 30% of control values after 4 days of exposure to 50 microg/liter 3, 4-dichloroaniline but remained unchanged by 0.5 microg/liter parathion. An approximately 1.3-fold induction of monooxygenase activities was caused by the model inducer naphthalene (0.1mg/liter). These results suggest that cytochrome P450-dependent monooxygenase activities may be useful variables in toxicity tests with aquatic insects.
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PMID:Altered cholinesterase and monooxygenase levels in Daphnia magna and Chironomus riparius exposed to environmental pollutants. 993 Dec 32

This study developed a bioassay with the isopod Porcellio dilatatus based on the activity of the enzymes acetylcholinesterase (AChE) and lactate dehydrogenase (LDH). The in vivo effects of the insecticides parathion-ethyl and endosulfan-sulfate on AChE and LDH activities of P. dilatatus under laboratory conditions were investigated. The route of uptake of the pesticides was through the food (alder leaves). Isopods were exposed to a wide range of concentrations of parathion or endosulfan (0.1, 1, 10, 25, 50, 100, 250, and 500 microg/g of food) for 21 days. After this period, the activity of AChE and LDH was determined. Parathion induced significant depression of both AChE and LDH activities. Animals fed with endosulfan-contaminated food exhibited lower LDH activities than control animals, while AChE activity was similar in all treatments. The results of the present investigation suggest that the isopod. P. dilatatus is a suitable species for use in toxicity tests and indicate that the enzymes AChE and LDH could be used as effect criteria both in laboratory and in field studies with this species.
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PMID:Novel bioassay based on acetylcholinesterase and lactate dehydrogenase activities to evaluate the toxicity of chemicals to soil isopods. 1058 Nov 23

Pesticide pollution in coastal ecosystems of Sinaloa, Mexico is considered to be a cause for slow growth, increase of diseases and sometimes massive mortality of shrimp. So it was necessary to develop fast techniques to detect pesticide pollution in shrimp habitats. Enzymatic and osmoregulation tests in shrimp exposed to DDT, Lindane, Chlordane, Lorsban, Gusathion, Folidol, Diazinon and Tamaron were carried out. Activity reductions from 11 to 2 units/ml in acetylcholinesterase and from 1 to 0 units/l in transaminases (GOT and GPT) were detected. Also increases in osmoregulation were observed in shrimp exposed to Folidol, Diazinon and Gusation, whereas decreases with DDT, Lindane and Lorsban at salinity 50/1000. We conclude that pesticides are causing alterations in these biochemical functions and this kind of tests represent a rapid and inexpensive method for pesticide pollution detection.
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PMID:Enzymatic and osmoregulative alterations in white shrimp Litopenaeus vannamei exposed to pesticides. 1066 12

Environmental chemicals may be involved in the etiology of breast cancers. Many studies have addressed the association between cancer in humans and agricultural pesticide exposure. Organophosphorous pesticides have been used extensively to control mosquito plagues. Parathion and malathion are organophosphorous pesticides extensively used to control a wide range of sucking and chewing pests of field crops, fruits, and vegetables. They have many structural similarities with naturally occurring compounds, and their primary target of action in insects is the nervous system; they inhibit the release of the enzyme acetylcholinesterase at the synaptic junction. Eserine, parathion, and malathion are cholinesterase inhibitors responsible for the hydrolysis of body choline esters, including acetylcholine at cholinergic synapses. Atropine, a parasympatholytic alkaloid, is used as an antidote to acetylcholinesterase inhibitors. The aim of this study was to examine whether pesticides were able to induce malignant transformation of the rat mammary gland and to determine whether alterations induced by these substances increase the cholinergic activation influencing such transformation. These results showed that eserine, parathion, and malathion increased cell proliferation of terminal end buds of the 44-day-old mammary gland of rats, followed by formation of 8.6, 14.3, and 24.3% of mammary carcinomas, respectively, after about 28 months. At the same time, acetylcholinesterase activity decreased in the serum of these animals from 9.78 +/- 0.78 U/mL in the control animals to 3.05 +/- 0.06 U/mL; 2.57 +/- 0.15 U/mL; and 3.88 +/- 0.44 U/mL in the eserine-, parathion-, and malathion-treated groups, respectively. However, atropine alone induced a significant (p < 0.05) decrease in the acetylcholinesterase activity from the control value of 9.78 +/- 0.78 to 4.38 +/- 0.10 for atropine alone, to 1.32 +/- 0.06 for atropine in combination with eserine, and 2.39 +/- 0.29 for atropine with malathion, and there was no mammary tumor formation. These results indicate that organophosphorous pesticides induce changes in the epithelium of mammary gland influencing the process of carcinogenesis, and such alterations occur at the level of nervous system by increasing the cholinergic stimulation.
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PMID:A rat mammary tumor model induced by the organophosphorous pesticides parathion and malathion, possibly through acetylcholinesterase inhibition. 1140 58

Parathion (PS) and chlorpyrifos (CPF) are organophosphorus insecticides, which elicit toxicity following biotransformation to the potent acetylcholinesterase inhibitors, paraoxon (PO) and chlorpyrifos oxon (CPO). Both oxons have also been shown to interact directly with muscarinic receptors coupled to inhibition of adenylyl cyclase. Immature animals are more sensitive than adults to the acute toxicity of PS and CPF but little is known regarding possible age-related differences in interactions between these toxicants and muscarinic receptors. We compared the inhibition of forskolin-stimulated cAMP formation by PO and CPO (1 nM-1 mM) in vitro in brain slices from 7-, 21-, and 90-day-old rats to the effects of well-known muscarinic agonists, carbachol and oxotremorine (100 microM). Both agonists inhibited cAMP formation in tissues from all age groups and both were more effective in adult and juvenile (20-26% inhibition) than in neonatal (12-13% inhibition) tissues. Atropine (10 microM) completely blocked agonist-induced inhibition in all cases. PO maximally inhibited (37-46%) cAMP formation similarly in tissues from all age groups, but atropine blocked those effects only partially and only in tissues from 7-day-old rats. CPO similarly inhibited cAMP formation across age groups (27-38%), but ATR was partially effective in tissues from all three age groups. Both oxons were markedly more potent in tissues from younger animals. We conclude that PO and CPO can directly inhibit cAMP formation through muscarinic receptor-dependent and independent mechanisms and that the developing nervous system may be more sensitive to these noncholinesterase actions.
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PMID:Inhibition of forskolin-stimulated cAMP formation in vitro by paraoxon and chlorpyrifos oxon in cortical slices from neonatal, juvenile, and adult rats. 1183 23

Environmental substances may be involved in the etiology of breast cancers. Many studies have found an association between cancer in humans and exposure to agricultural pesticides. Organophosphorous pesticides have been used to control mosquito plagues. Parathion and malathion, organophosphorous pesticides are cholinesterase inhibitors responsible for the hydrolysis of body choline esters, including acetylcholine at cholinergic synapses. Their primary target of action in insects is the nervous system whereby they inhibit the enzyme acetylcholinesterase at synaptic junction. Atropine is a parasympatholytic alkaloid used as an antidote to acetylcholinesterase inhibitors. We have established an experimental breast cancer model, where epithelial cells in the rat mammary gland underwent a stepwise transformation into malignant cells by exposure to pesticides (Cabello et al, 2001). The aim of this work was to examine whether pesticides were able to induce progression of malignant transformation of a human breast epithelial cell line, MCF7. These results showed that parathion and malathion increased PCNA and induced mutant p53 protein expression of MCF7 cells in comparison to controls and atropine inhibited such action. These results indicated that organophosphorous pesticides can induce more changes in this malignant breast cell line, inducing another step in the progression of the transformation process and atropine on the other hand inhibited the effect of such substances.
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PMID:Organophosphorous pesticides in breast cancer progression. 1276 45

This report describes the development of novel sonochemically fabricated, bioengineered acetylcholinesterase and polyaniline carbon/cobalt phthalocyanine biosensors for the ultra-sensitive determination of a number of different pesticides. Arrays of this type typically have population micro-electrode densities of up to approximately 2 x 10(5) cm(-2); these represent the highest micro-electrode population densities reported to date by any fabrication means. The enzymatic response of the sensors is inhibited upon incubation with the pesticide, and we have shown that Dichlorvos, Parathion and Azinphos may be determined down to concentrations of approximately 1 x 10(-17) M, approximately 1 x 10(-16) M and approximately 1 x 10(-16) M, respectively. These lower limits of detection are lower than otherwise achievable by any other analytical approach. Measurements were performed within a custom built flow injection system that operates at a constant flow of 1 ml min(-1). Sensor stability studies were also performed whereby a stabilizer mixture of sucrose and polygalacturonic acid was added to the immobilised enzyme matrix at the working electrode and left to dry. Sixty-five percent of the initial enzyme activity was found to remain after a period of 92 days to allow storage of these electrodes and facilitating transportation if required.
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PMID:Sonochemically fabricated acetylcholinesterase micro-electrode arrays within a flow injection analyser for the determination of organophosphate pesticides. 1574 Oct 58

We developed a polymerized crystalline colloidal array (PCCA) photonic crystal sensing material that senses the organophosphorus compound parathion at ultratrace concentrations in aqueous solutions. A periodic array of colloidal particles is embedded in a hydrogel network with a lattice spacing such that it Bragg diffracts visible light. The molecular recognition agent for the sensor is the enzyme acetylcholinesterase (AChE), which binds organophosphorus compounds irreversibly, creating an anionic phosphonyl species. This charged species creates a Donnan potential, which swells the hydrogel network, which increases the embedded particle array lattice spacing and causes a red-shift in the wavelength of light diffracted. The magnitude of the diffraction red-shift is proportional to the amount of bound parathion. These AChE-PCCAs act as dosimeters for parathion since it irreversibly binds. Parathion concentrations as low as 4.26 fM are easily detected.
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PMID:Acetylcholinesterase-based organophosphate nerve agent sensing photonic crystal. 1576 62

Organophosphorous pesticides are currently widely used in China to help boost agricultural production. However, these pesticides pose various threats to organisms, including humans, and are thus a cause of concern. Five organophosphorous pesticides, monocrotophos, omethoate, parathion-methyl, phoxim and dichlorvos, were examined for their effects on mammalian cell lines to determine their potential impact on physiological functions in vivo. Results show an increased proliferation of MCF-7 cells treated with 0.2 microM monocrotophos or 0.4 microM omethoate, suggesting that these compounds can induce breast cancer cell proliferation at relatively low concentrations. Murine primary spleen cells markedly decreased in number starting at a pesticide concentration of 0.01 microM; no cytotoxicity was observed below 0.001 microM. BALB/c3T3 murine fibroblasts treated with 0.25 microM monocrotophos showed enhanced DNA synthesis, while those treated with the other pesticides showed results similar to that of the control. The different pesticides reduced the acetylcholinesterase (AChE) activity of the rat neuronal cell line PC12 in a dose-dependent manner up to 100 microM. Parathion-methyl and phoxim showed acute toxicity at 0.01 microM. Finally, phoxim and parathion-methyl significantly reduced the transepithelial electrical resistance (TEER) of human intestinal Caco-2 cells, indicating that these pesticides can disrupt the tight-junction permeability of cell monolayers. These in vitro assays, which are rapid, reproducible, simple and inexpensive, clearly show the effects of organophosphorous pesticides on mammalian cells and suggest the potential impact of these pesticides on organisms in vivo.
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PMID:Effects of organophosphorous pesticides used in china on various mammalian cells. 1579 57

Glucose feeding can markedly exacerbate the toxicity of the anticholinesterase insecticide, parathion. We determined the effects of parathion on brain nitric oxide and its possible role in potentiation of toxicity by glucose feeding. Adult rats were given water or 15% glucose in water for 3 days and challenged with vehicle or parathion (18 mg/kg, s.c.) on day 4. Functional signs, plasma glucose and brain cholinesterase, citrulline (an indicator of nitric oxide production) and high-energy phosphates (HEPs) were measured 1-3 days after parathion. Glucose feeding exacerbated cholinergic toxicity. Parathion increased plasma glucose (15-33%) and decreased cortical cholinesterase activity (81-90%), with no significant differences between water and glucose treatment groups. In contrast, parathion increased brain regional citrulline (40-47%) and decreased HEPs (18-40%) in rats drinking water, with significantly greater changes in glucose-fed rats (248-363% increase and 31-61% decrease, respectively). We then studied the effects of inhibiting neuronal nitric oxide synthase (nNOS) by 7-nitroindazole (7NI, 30 mg/kg, i.p. x4) on parathion toxicity and its modulation by glucose feeding. Co-exposure to parathion and 7NI led to a marked increase in cholinergic signs of toxicity and lethality, regardless of glucose intake. Thus, glucose feeding enhanced the accumulation of brain nitric oxide following parathion exposure, but inhibition of nitric oxide synthesis was ineffective at counteracting increased parathion toxicity associated with glucose feeding. Evidence is therefore presented to suggest that nitric oxide may play both toxic and protective roles in cholinergic toxicity, and its precise contribution to modulation by glucose feeding requires further investigation.
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PMID:Modulation of parathion toxicity by glucose feeding: Is nitric oxide involved? 1717 40


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