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 effect of two different doses (1 microg and 50 microg Se/100 g body wt) of selenium on quinolinic acid toxicity was investigated in rat's brain. Male albino rats were maintained for 60 days as follows: (1) control group (normal diet), (2) Quinolinic acid group (55 microg/100 g body wt)/day, (3) high dose selenium (50 microg/100 g body wt)/day, (4) high dose selenium ((50 microg/100 g body wt) + Quinolinic acid (55 microg/100 g body wt)/day (5) low dose selenium (1 microg/100 g body wt)/day and (6) low dose selenium (1 microg/100 g body wt) + Quinolinic acid (55 microg/100 g body wt)/day. Results revealed that quinolinic acid intake lead to an increase in the oxidative stress as evidenced by decreased activity of antioxidant enzymes (SOD, catalase and GR), increased amount of lipid peroxidation products (MDA,HP and CD) and free fatty acids compared to control group. Co administration of selenium at a dose of 1 microg/100 g body wt along with quinolinic acid had reduced the oxidative stress induced by quinolinic acid and it also led to a change in the brain architecture as evidenced by the decreased activity of acetyl cholinesterase and decreased concentration of neurotransmitters. Histopathological studies revealed that selenium at a dose of 1 microg was more effective in reducing the oxidative stress and higher dose of selenium was toxic.
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PMID:Impact of co administration of selenium and quinolinic acid in the rat's brain. 1946 74

Intracerebroventricular (ICV) streptozotocin (STZ) has been shown to cause cognitive impairment, which is associated with increased oxidative stress in the brain of rats. In the present study, we investigated the effect of both the isoforms of vitamin E, alpha-tocopherol and tocotrienol against ICV STZ-induced cognitive impairment and oxidative-nitrosative stress in rats. Adult male Wistar rats were injected with ICV STZ (3 mg/kg) bilaterally. The learning and memory behavior was assessed using Morris water maze and elevated plus maze. The rats were sacrificed on day 21 and parameters of oxidative stress, nitrite levels and acetylcholinesterase activity were measured in brain homogenate. alpha-Tocopherol as well as tocotrienol treated groups showed significantly less cognitive impairment in both the behavioral paradigms but the effect was more potent with tocotrienol. Both isoforms of vitamin E effectively attenuated the reduction in glutathione and catalase and reduced the malonaldehyde, nitrite as well as cholinesterase activity in the brains of ICV STZ rats in a dose dependent manner. The study demonstrates the effectiveness of vitamin E isoforms, of which tocotrienol being more potent in preventing the cognitive deficits caused by ICV STZ in rats and suggests its potential in the treatment of neurodegenerative diseases such as Alzheimer's disease.
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PMID:Chronic treatment with tocotrienol, an isoform of vitamin E, prevents intracerebroventricular streptozotocin-induced cognitive impairment and oxidative-nitrosative stress in rats. 1946 15

The use of a very effective insecticide against sucking pests, neonicotinoid imidacloprid, has been increasing extensively. For this reason elevated concentrations are expected in aquatic environment. Despite this fact, there is still a lack of data available on its possible risk for the environment. In this study, the potential hazards of imidacloprid and its commercial product Confidor SL 200 to aquatic environment were identified by the acute and chronic toxicity assessment using bacteria Vibrio fischeri, algae Desmodesmus subspicatus, crustacean Daphnia magna, fish Danio rerio and the ready biodegradability determination. We found out, that imidacloprid was not highly toxic to tested organisms in comparison to some other environmental pollutants tested in the same experimental set-up. Among the organisms tested, water flea D. magna proved to be the most sensitive species after a short-term (48 h EC50=56.6 mg L(-1)) and long-term exposure (21 d NOEC=1.25 mg L(-1)). On the contrary, the intensified toxicity of Confidor SL 200 in comparison to analytical grade imidacloprid was observed in the case of algae and slight increase of its toxicity was detected testing daphnids and fish. The activities of cholinesterase, catalase and glutathione S-transferase of daphnids were not early biomarkers of exposure to imidacloprid and its commercial product. Imidacloprid was found persistent in water samples and not readily biodegradable in aquatic environment. Due to increased future predicted use of commercial products containing imidacloprid and the findings of this work, we recommend additional toxicity and biodegradability studies of other commercial products with imidacloprid as an active constituent.
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PMID:Hazard identification of imidacloprid to aquatic environment. 1950 10

We studied the effects of combined exposure to arsenic and fluoride on (i) brain biogenic amines, oxidative stress and its correlation with glutathione and linked enzymes; (ii) alterations in the structural integrity of DNA; and (iii) brain and blood arsenic and fluoride levels. Efficacy of alpha-tocopherol in reducing these changes was also determined. Male mice were exposed to sodium meta arsenite (50 ppm) and sodium fluoride (50 ppm) individually and in combination for ten weeks. Animals were given vitamin E supplementation (5 mg/kg, i.m., alternate days) throughout the experiment. Exposure to arsenic and fluoride significantly decreased the levels of brain biogenic amines. However; acetyl cholinesterase (AChE) and monoamine oxidase (MAO) activities showed an increase on fluoride exposure. There was also an increase in reactive oxygen species, thiobarbituric acid reactive species level, glutathione S-transferase and glutathione peroxidase activities and decreased superoxide dismutase activity, GSH:GSSG ratio, glucose 6-phosphate dehydrogenase activity. Combined exposure to these toxicants produced more pronounced effects on AChE, MAO, SOD and catalase activities. Infrared spectra showed less toxicity during combined exposure as the characteristic peaks of cytosine and alpha-helical structure of DNA were observed in normal and arsenic plus fluoride-exposed animals. Vitamin E reduced brain fluoride level and tissue oxidative stress but had no effect on arsenic. Combined exposure to arsenic and fluoride does not necessarily lead to more pronounced toxicity and interestingly exhibit some antagonistic effects. Vitamin E supplementation may be of added value in reverting some of the toxic effects.
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PMID:Co-exposure to arsenic and fluoride on oxidative stress, glutathione linked enzymes, biogenic amines and DNA damage in mouse brain. 1963 23

Neurotoxic and cytotoxic effects of venoms from Scorpio maurus palmatus taken from different populations were assessed for geographic based variability in toxicity, and to evaluate their insecticidal potency. Scorpions were collected from four regions. Three locations were mutually isolated pockets in the arid area of Southern Sinai. The fourth sample was collected from a population inhabiting the semi-arid environment of Western Mediterranean Coastal Desert. The neurotoxic (paralytic) effect of the venom from each population was assayed by its ability to induce permanent disability in adult cockroaches within 3h. Venom was applied using microinjection techniques through an intersegmental membrane. Probit analysis was used to calculate the Paralytic Effective Dose (PED(50), ng/100mg). Levels of glutathione, lipid peroxidation, protein carbonyl content and nitric oxide, as well as the activities of superoxide dismutase, catalase and cholinesterase, were measured to assess the cytotoxicity of the venom. The results show that the injected venom from each population induced obvious spasticity, followed by flaccid paralysis. All the tested biochemical parameters, except glutathione content, revealed significant differences in toxicity in venom taken from the different scorpion populations. We conclude that (i) the venom of this scorpion has significant neurotoxic and cytotoxic effects on insect cells, (ii) its efficacy, as assessed by the PED(50) unit, exhibited variation across its geographic range, and (iii) components in the venom may have the potential for being developed into effective and environmentally friendly bioinsecticides.
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PMID:Neurotoxic and cytotoxic effects of venom from different populations of the Egyptian Scorpio maurus palmatus. 1968 84

In the present study we report data obtained from the evaluation of subjects occupationally exposed to pesticide mixtures from Santa Fe province, Argentina, using biomarkers for butyrylcholinesterase (BChE) and acetylcholinesterase (AChE) activities, catalase (CAT), lipid peroxidation (by TBARS assay) and the Damage Index Comet Assay (DICA). Our results showed an AChE inhibition (25% and 15% in directly and indirectly groups, respectively) in relation to controls with no significant modifications in BChE. TBARS levels were higher (51%) in pesticide sprayers while CAT activity was reduced in both, applicators (61%) and non-applicators (43%). DICA was significantly increased in direct (83%) and indirect (98%) exposed groups, compared with controls. These results showed modifications in lipid peroxidation, antioxidant defence system, and DNA damage in lymphocytes of exposed workers. Further investigations are suggested in order to link our findings with adverse health effects observed in chronic pesticide toxicity, where oxidative damage plays a pathophysiological role.
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PMID:Biomarkers of cellular reaction to pesticide exposure in a rural population. 1981 Nov 13

The authors studied influence of vibration on some serum biochemical values. Oxidative stress and muscular tissue parameters appeared to be the earliest indicators to change. Preclinical stage of vibration disease is characterized by lower activity of superoxide dismutase, increased urinary levels of creatinine and CCr coefficient. Slight increase in serum catalase activity is seen. These parameters increase in vibration disease patients. Urinary creatinine level remains high in some individuals with residual manifestations of vibration disease, after the exposure. Serum levels of copper, ceruloplasmin, potassium, sodium, cholinesterase activity are changed insignificantly under influence of vibration. The authors calculated occurrence of individuals who demonstrate abnormal changes of the stated parameters.
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PMID:[Biochemical markers of vibration effects in workers, and their criterial evaluation]. 2015 97

The activity of cholinesterase (ChE), glutathione-S transferase (GST), glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PDH) and catalase (CAT) was evaluated in the gill and digestive glands of the Perna perna mussel transplanted to three non-contaminated mariculture zones under the influence of distinct physical-chemical characteristics. Differences among sites for ChE, GST and CAT activities in gill, as well as ChE, GST and G6PDH activity in digestive gland of mussels, were found and possibly related to differences in physicochemical characteristics of the sites and/or biological status of the mussels. Mussels that were transplanted to another, more urbanized site (Ponta do Lessa) with similar physicochemical characteristics to one of the farming sites (Sambaqui), was also chosen to evaluate biomarker responses to pollution. Activities of ChE, GST and GR in the digestive glands and CAT in the gills were higher in the polluted site. GR was the only biomarker to be unaltered in different farming sites, but induced in the pollution site. The trace metal concentrations in the mussels were low and unlikely to cause the changes observed in the biomarker levels. The present study strongly suggests that monitoring programs should compare sites with similar physicochemical characteristics when using a complementary biomarker approach. In addition, the baselines for the biomarkers and metal used in the present study can serve as a reference for the monitoring of these mariculture zones in future monitoring programs employing P. perna.
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PMID:Biochemical biomarkers and metals in Perna perna mussels from mariculture zones of Santa Catarina, Brazil. 2038 Nov 45

The present study was undertaken to establish mode of action, comparative therapeutic efficacy and safety evaluation of N-acetyl cysteine and dithiothreitol against acute dimethylmercury poisoning in rats. Male Sprague-Dawley albino rats (150 +/- 10 g) were randomly divided into six groups. Group 1 served as control. Group 2-4 were administered dimethylmercury (10 mg/kg, p.o.) once only and group 2 served as experimental control. Animals of group 3 and 4 were received N-acetyl cysteine and dithiothreitol. Compared to the control, significant increase (p < or = 0.05) was observed in the activities of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lipid peroxidation level and mercury ion concentration, however reduced glutathione, catalase, adenosine triphosphatase, acetyl cholinesterase (in brain only) were also decreased. It was concluded that N-acetyl cysteine provided maximum protection when compared with dithiothreitol group.
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PMID:Protective role of thiol chelators against dimethylmercury induced toxicity in male rats. 2040 49

Acute dose of lindane (40 mg/kg body weight, ip) caused significant reduction in butyrylcholinesterase (BChE) activity both in olfactory lobe and cerebrum of mice along with reduction in catalase (CAT), total protein and elevation in superoxide dismutase (SOD) and cholesterol contents. Pretreatment by a combination of antioxidants, vitamin E, vitamin C, a- lipoic acid and stilbene resveratrol (125 mg/kg body weight, ip) significantly augment the altered level of BChE and protect the other parameters in both the brain regions. The results were adequately in agreement with the histochemical findings, suggesting the neuroprotective efficacy of combination of antioxidants studied on the lindane induced neurotoxicity.
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PMID:Ameliorative effect of a combination of vitamin E, vitamin C, alpha-lipoic acid and stilbene resveratrol on lindane induced toxicity in mice olfactory lobe and cerebrum. 2045 24


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