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)

Dimethoate, an organophosphate pesticide, is used in controlling the pests of a variety of crops. The study was carried out to understand the role of dimethoate in inducing oxidative stress leading to generation of free radicals and alterations in antioxidant enzymes and scavengers of oxygen free radicals. The effects of subchronic exposure of dimethoate in the production of oxidative stress were evaluated in male Wistar rats in the present study. Dimethoate was administered orally at doses 0.6, 6, and 30 mg/kg for 30 days in these rats. The results indicated an increase in levels of hepatic Cytochrome P450, lipid peroxidation, catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase in liver and brain at doses 6 and 30 mg/kg. There were no significant changes in the level of glucose-6-phosphate dehydrogenase activity except in liver at 30 mg/kg. A decrease in glutathione was observed at 30 and 6 mg/kg in both liver and brain. Glutathione-S-transferase increased at 30 and 6 mg/kg in liver and 30 mg/kg in brain. Erythrocyte acetylcholinesterase was inhibited at 30 and 6 mg/kg doses. Dose-dependent histopathological changes were seen in both liver and brain. This study concludes that oxidative stress due to dimethoate may be ascribed to induction of Cytochrome P450, inhibition of AChE and disturbance in activities of GSH and GST enzymes causing lipid peroxidation and histological and electron microscopic changes in liver and brain.
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PMID:Dimethoate-induced effects on antioxidant status of liver and brain of rats following subchronic exposure. 1611 89

Crassostrea rhizophorae is a euryhaline oyster that inhabits mangrove areas, which are widely distributed along the Brazilian coast. The aim of this study was to investigate the effects of salinity (9, 15, 25, and 35ppt) on the activities of glutathione S-transferase (GST), glucose 6-phosphate dehydrogenase (G6PDH), catalase (CAT), and acetylcholinesterase (AChE) in the digestive gland of this species after exposure to diesel oil for 7 days at nominal concentrations of 0.01, 0.1, and 1mlL(-1) and after depuration for 24h and 7 days. GST activity increased in a diesel oil concentration-dependent manner at salinities 25 and 15ppt and remained slightly elevated even after depuration periods of 24h and 7 days. No changes were observed in the activities of G6PDH, CAT, and AChE in the oysters exposed to diesel and depurated. Based on these results, GST activity in the digestive gland of C. rhizophorae might be used as a biomarker of exposure to diesel oil in sites where the salinity is between 15 and 25ppt, values usually observed in mangrove ecosystems.
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PMID:Effects of salinity on biomarker responses in Crassostrea rhizophorae (Mollusca, Bivalvia) exposed to diesel oil. 1621 31

This investigation gives detailed analysis of peripheral marker enzymes as well as neurobehavioral tests following chronic aluminium (Al) exposure (10 mg/kg b.w. for 12 weeks intragastrically). We observed a significant decrease in the levels of serum cholinesterase after toxicity. The enzymatic activity of cytochrome oxidase (CO), the terminal enzyme of the electron transport chain, was significantly diminished and that of glucose-6-phosphate dehydrogenase (G-6-PD) was significantly enhanced. Neuromuscular co-ordination was assessed using motor and memory function tests. Deficits were observed suggesting a probable model for chronic Al neurotoxicity.
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PMID:Possible peripheral markers for chronic aluminium toxicity in Wistar rats. 1657 10

Erythrocytes are excellent models for the study of interactions of xenobiotics with biomembranes. Present work is designed to study the in vitro effects of some organophosphates (ethion, chlorpyrifos, dimethoate and monocrotophos) on rat erythrocytes. Treatment of erythrocytes with organophosphates resulted in decreased erythrocyte glucose-6-phosphate dehydrogenase (G-6-PD) activity, whereas activities of glutathione-s-transferase (GST) and glutathione reductase (GR) were increased. Reduced Glutathione (GSH) content of RBCs was decreased after treatment with the pesticides. Increased activities of GST and GR were due to induction of natural defense mechanism of erythrocytes against the toxicity of the pesticides. Membrane bound enzymes like acetylcholinesterase (AChE), Na(+)-K(+)-ATPase and Ca(2+)-ATPase were also inhibited. Altered activities of these enzymes along with decreased GSH content indicate increased oxidative stress in erythrocytes after treatment with organophosphates.
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PMID:Erythrocyte antioxidant enzymes in toxicological evaluation of commonly used organophosphate pesticides. 1687 49

Sodium monofluoroacetate (compound 1080) is one of the most potent pesticides. It is also a metabolite of many other fluorinated compounds, including anticancer agents, narcotic analgesics, pesticides or industrial chemicals. Other sources of water contamination are the atmospheric degradation of hydrofluorocarbons and hydrochlorofluorocarbons. However, there is little information available about the adverse effects of sodium fluoroacetate in aquatic organisms. Firstly, the bacterium Vibrio fischeri (decomposer), the alga Chlorella vulgaris (1st producer) and the cladoceran Daphnia magna (1st consumer) were used for the ecotoxicological evaluation of SMFA. The most sensitive models were C. vulgaris and D. magna, with a NOAEL of 0.1 and an EC50 of 0.5 mM at 72 h, respectively. According to the results after the acute exposure and due to its high biodegradation rate and low bioaccumulation potential, sodium fluoroacetate is most unlikely to produce deleterious effects to aquatic organisms. Secondly, two fish cell lines were employed to investigate the effects and mechanisms of toxicity in tissues from 2nd consumers. The hepatoma fish cell line PLHC-1 was more sensitive to SMFA than the fibroblast-like fish cell line RTG-2, being the uptake of neutral red the most sensitive bioindicator. Lysosomal function, succinate dehydrogenase and acetylcholinesterase activities were inhibited, glucose-6-phosphate dehydrogenase activity was particularly stimulated, and metallothionein and ethoxyresorufin-O-deethylase levels were not modified. Intense hydropic degeneration, macrovesicular steatosis and death mainly by necrosis but also by apoptosis were observed. Moreover, sulphydryl groups and oxidative stress could be involved in PLHC-1 cell death induced by SMFA more than changes in calcium homeostasis.
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PMID:Ecotoxicological evaluation of sodium fluoroacetate on aquatic organisms and investigation of the effects on two fish cell lines. 1715 55

Gemfibrozil is a lipid-regulating agent widely used in patients at risk of coronary disease. Pharmaceutical products, such as gemfibrozil, are found in municipal effluents and represent a major source of contamination. To date, there is little available information about the adverse effects of gemfibrozil in aquatic organisms. For this reason, the toxic effects were investigated using model systems from four trophic levels. The most sensitive system was the immobilization of Daphnia magna, with a non-observed adverse effect level of 30 microM and a mean effective concentration of 120 microM after 72 h, followed by the inhibition of bioluminescence of Vibrio fischeri, the hepatoma fish cell line PLHC-1 line and the inhibition of the growth of Chlorella vulgaris. Although protein content, neutral red uptake, methylthiazol metabolization and lysosomal function were reduced in PLHC-1 cells, stimulations were observed for lysosomal function, metallothionein levels and succinate dehydrogenase, glucose-6-phosphate dehydrogenase and acetylcholinesterase activities. No changes were observed in ethoxyresorufin-O-deethylase activity. The main morphological alterations were hydropic degeneration and loss of cells. Modulation studies on gemfibrozil toxicity were also carried out. General antioxidants and calcium chelators did not modify the toxicity of gemfibrozil, whereas a Fe(III) chelator, a membrane permeable sulphydryl-protecting compound and glutathione level modifying agents did change the toxicity. One of the possible mechanisms of gemfibrozil toxicity seems to be the binding to sulphydryl groups, including those of glutathione. According to the result, gemfibrozil should be classified as harmful to aquatic organisms. However, comparing the concentrations in water and the toxicity quantified in the assayed systems, gemfibrozil is not expected to represent acute risk to the aquatic biota.
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PMID:Toxicological effects of the lipid regulator gemfibrozil in four aquatic systems. 1716 44

Propyl gallate is an antioxidant widely used in foods, cosmetics and pharmaceuticals. The occurrence and fate of additives in the aquatic environment is an emerging issue in environmental chemistry. To date, there is little available information about the adverse effects of propyl gallate on aquatic organisms. Therefore, the toxic effects were investigated, using five model systems from four trophic levels. The most sensitive system was the hepatoma fish cell line PLHC-1 according to total protein content, with an EC(50) of 10 microM and a NOAEL of 1 microM at 72 h, followed by the immobilization of Daphnia magna, the inhibition of bioluminescence of Vibrio fischeri, the salmonid fish cell line RTG-2 and the inhibition of the growth of Chlorella vulgaris. Although protein content, neutral red uptake, methylthiazol metabolization and acetylcholinesterase activity were reduced in PLHC-1 cells, stimulations were observed for lysosomal function, succinate dehydrogenase, glucose-6-phosphate dehydrogenase and ethoxyresorufin-O-deethylase activities. No changes were observed in metallothionein levels. The main morphological observations were the loss of cells and the induction of cell death mainly by necrosis but also by apoptosis. The protective and toxic effects of propyl gallate were evaluated. General antioxidants and calcium chelators did not modify the toxicity of propyl gallate, but an iron-dependent lipid peroxidation inhibitor gave 22% protection. The results also suggest that propyl gallate cytotoxicity is dependent on glutathione levels, which were modulated by malic acid diethyl ester and 2-oxothiazolidine-4-carboxylic acid. According to the results, propyl gallate should be classified as toxic to aquatic organisms.
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PMID:Ecotoxicological effects of the antioxidant additive propyl gallate in five aquatic systems. 1738 89

Determination of erythrocyte number and their indices and enzymatic activity of: glucose-6-phosphate dehydrogenase (G-6PD), superoxide dismutase (SOD), acetylcholinesterase (AchE), glutathione reductase (GR) and hexokinase (Hx) in peripheral blood erythrocytes of workers chronically exposed to mercury vapours during the production of chloride (the mercuric electrolysis method). The studied workers were equipment operators, electricians and electrolysis maintenance men at the chloride production department using the mercuric electrolysis method. The study involved 46 men, aged 21 to 56, (x = 39 +/- 10.4) exposed to mercury vapours for the period from 7 months to 32 years (x = 14.7+/-10.8), working in a three shift system, for 8 hours a day. Smokers constituted 50% of the studied group (23 men). Urine mercury concentrations of workers exposed to mercury vapours were in the range from 10 to 215 microg/dm3 (x = 81,4 +/- 72,9) and in blood in range 4 do 72 microg/dm3 (x=16.3 +/- 15,0). Controls were 46 men aged 20-54, (x=33.6 +/- 9.8), workers and voluntary blood donors, who never experienced occupational exposure to mercury vapours or other chemicals, and to physical agents. The percentage of smokers in the control group was 34.7% (16 men). Basic haematological determinations (hematocrit - Hct, Hb concentration, erythrocyte number in mm3 of blood, mean red cell hemoglobin concentration (MCHC), mean red cell volume (MCV) and enzymatic studies (activity of G-6PD, SOD, AchE, GR, Hx) in peripheral blood samples obtained from workers and controls were performed. Hematological parameters of the peripheral blood were determined using AVL 808 hematological counter, following the manufacturer's instructions. Activity of the studied enzymes was estimated by the spectrophotometric method described by Beutler, following the recommendations of the International Committee for Standardisation in Hematology. Values of Ht were higher in all the subgroups exposed to Hg workers (divided according to duration of exposure or urine mercury concentrations) in comparison to the control group. The erythrocyte number in mm3 of peripheral blood was also higher in the exposed workers group than in controls. MCHC in the total group exposed to mercury vapours was lower than in the controls. In the subgroup exposed to mercury vapours for < 10 years, the value of this parameter was lower than in the control group; whereas in the subgroups separated in respect to mercury concentration in the urine, it was lower only in workers showing the highest urine concentration of this metal. In workers exposed to mercury vapours, MCV index values were lower than in the controls. In the subgroups of workers who smoked and those who did not smoke, they were also lower than in the controls; whereas in the group of the longest exposed workers from 21 to 35 years, it was found to be higher than in controls. The activity of G6PD was lower in the group of subjects occupationally exposed to mercury vapours than in the control group - 5.60 +/- 1.60 and 7.41 +/- 0.43 IU/gHb respectively. When comparing the subgroups of smokers and non-smokers with the controls, workers showed lower G6PD activity than in the matching control subgroups - 6.24 +/- 1.97 and 7.44 +/-0.22 IU/gHb in the subgroups of smokers and 4.97 +/- 0.72 and 7.38 +/- 0.18 IU/gHb in non-smokers respectively. Erythrocyte G6PD activity was lower in all studied groups separated in respect to exposure time - 5.54 +/- 1.75, 6.02 +/- 2.05 and 5.54 +/- 1.05 IU/gHb respectively. The same pattern of changes was observed in the subgroups separated in respect to mercury concentration in the urine compared to the controls. The lowest enzyme activity was found in the subgroups showing the highest mercury concentration in the urine wnen compared with the subgroup with the lowest urine concentration of this metal - 5.19 +/- 1.50 and 6.00 +/- 1.84 IU/gHb respectively SOD activity in the group of workers exposed to mercury was lower compared to the controls - 2289.97 +/- 122.31 and 2418.03 +/- 60.28 IU/gHb respectively. The smoking and non-smoking workers showed respective SOD activities on - 2305.43 +/- 102.75 and 2274.50 +/- 124.5 IU/gHb; whereas in the matching subgroup of controls - 2452.11 +/- 88.72 and 2382.09 +/- 91.22 IU/gHb, respectively. The activity of this enzyme in all investigated groups selected in respect to length of employment, revealed lower values when compared with the controls - 2271.20 +/- 115.23 in the group with under 10 years of exposure, 2335.11 +/-167.71 IU/gHb in those exposed for 11-20 years, and 2290.40 +/- 26.12 IU/gHb in the subgroup exposed for the longest period of time. Similar changes were observed in the activity of this enzyme in the subgroups separated in respect to mercury concentration in the urine when SOD activity was compared with the controls. The AchE activity was higher in the group exposed to mercury vapours compared to the controls and the respective values were - 50.22 +/- 14.44 and 36.87 +/- 2.92 IU/gHb. In the subgroups separated in respect to length of exposure, the activity of this enzyme was statistically significantly higher than in the control group. The GR activity levels were lower in the exposed group - 8.01 +/-2.54 IU/gHb, compared to the controls - 10.24 +/- 1.24 IU/gHb. In the subgroups of smokers and non-smokers, GR activity was lower, 8.48 +/- 2.37 and 7.54 +/- 2.68 IU/gHb, compared to smokers and non-smokers in the control group, 10.26 +/- 1.01 and 10.16 +/- 1.03 IU/gHb, respectively. The GR activity was also statistically significantly lower in all groups separated in respect to duration of exposure, with the values of 8.56 +/-2.39, 8.26 +/- 2.38, 7.06 +/- 2.75 IU/gHb, respectively in subject groups and 10.24 +/- 1.35 in the control group. Similar changes were noticed in the subgroup separated in respect to mercury concentration in the urine. The Hx activity was lower in the group exposed to mercury vapours - 1.08 +/-0.11. compared with the controls - 1.21 +/- 0.16 IU/gHb. The enzyme activity showed a similar pattern in the subgroups separated in respect to duration of exposure when they were compared with the control group. Exposure to mercury vapours present changes in the red blood cells, manifested by increased (when compared with the control group), number of erythrocytes in peripheral and decreased mean cell volume and mean cell hemoglobin concentration values, as well as changes in the metabolic processes occurring in the erythrocytes. In subjects exposed to mercury vapours some metabolic processes may be additionally modified by addiction to cigarette smoking.
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PMID:[Red cell system and selected red cell enzymes in men occupationally exposed to mercury vapours]. 1778 49

Indium nitrate is mainly used as a semiconductor in batteries, for plating and other chemical and medical applications. There is a lack of available information about the adverse effects of indium compounds on aquatic organisms. Therefore, the toxic effects on systems from four trophic levels of the aquatic ecosystem were investigated. Firstly, the bacterium Vibrio fischeri, the alga Chlorella vulgaris and the cladoceran Daphnia magna were used in the toxicological evaluation of indium nitrate. The most sensitive model was V. fischeri, with a NOAEL of 0.02 and an EC(50) of 0.04 mM at 15 min. Although indium nitrate should be classified as harmful to aquatic organisms, it is not expected to represent acute risk to the aquatic biota. Secondly, PLHC-1 fish cell line was employed to investigate the effects and mechanisms of toxicity. Although protein content, neutral red uptake, methylthiazol metabolization, lysosomal function and acetylcholinesterase activity were reduced in cells, stimulations were observed for metallothionein levels and succinate dehydrogenase and glucose-6-phosphate dehydrogenase activities. No changes were observed in ethoxyresorufin-O-deethylase activity. To clarify the main events in PLHC-1 cell death induced by indium nitrate, nine modulators were applied. They were related to oxidative stress (alpha-tocopherol succinate, mannitol and sodium benzoate), disruption of calcium homeostasis (BAPTA-AM and EGTA), thiol protection (1,4-dithiotreitol), iron chelation (deferoxiamine) or regulation of glutathione levels (2-oxothiazolidine-4-carboxylic acid and malic acid diethyl ester). The main morphological alterations were hydropic degeneration and loss of cells. At least, in partly, toxicity seems to be mediated by oxidative stress, and particularly by NADPH-dependent lipid peroxidation.
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PMID:Toxicological assessment of indium nitrate on aquatic organisms and investigation of the effects on the PLHC-1 fish cell line. 1780 41

Azinphos-methyl is an organophosphate insecticide used for pest control on a number of food crops in many parts of the world. The oligochaete Lumbriculus variegatus and pigmented and non-pigmented specimens of the gastropod Biomphalaria glabrata are freshwater invertebrates that have been recommended for contamination studies. Recently, it has been shown that L. variegatus worms exhibit a higher cholinesterase (ChE) activity and a greater sensitivity to in vivo ChE inhibition by azinphos-methyl than pigmented B. glabrata snails. The aims of the present study were (1) to investigate if, in addition to its anticholinesterase action, azinphos-methyl has also pro-oxidant activity in L. variegatus and B. glabrata, and (2) to examine if species that are highly susceptible to the neurotoxic effects of organophosphates also suffer a greater degree of oxidative stress. Therefore, total glutathione (t-GSH) levels and activities of cholinesterase (ChE), superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and glucose 6-phosphate dehydrogenase (G6PDH) were measured in the whole body soft tissue of organisms exposed for 48 and 96 h to a level of azinphos-methyl that produces 50% of inhibition on ChE. Results showed different patterns of antioxidant responses between the gastropods and the oligochaetes, and even between the two phenotypes of gastropods: (1) in exposed L. variegatus t-GSH levels increased and CAT and SOD activities decreased with respect to control organisms, (2) in pigmented gastropods, SOD decreased while CAT transiently diminished, and (3) in non-pigmented gastropods, SOD activity showed a biphasic response. GST and G6PDH were not altered by azinphos-methyl exposure. Of note, t-GSH levels were 4-fold times higher in L. variegatus than in both phenotypes of B. glabrata. This may suggest that GSH could play a more important role in antioxidant defense in L. variegatus than in B. glabrata.
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PMID:Effects of azinphos-methyl exposure on enzymatic and non-enzymatic antioxidant defenses in Biomphalaria glabrata and Lumbriculus variegatus. 1853 25


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