Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Longitudinal studies were carried out over 55 weeks in vitamin E deficient and control rats. It was shown that neurological tissues (brain, cord and nerve) retained a greater percentage of vitamin E (alpha-tocopherol) than other tissues (serum, liver and adipose tissue), and that there was no evidence for compensation by other antioxidant enzyme systems (superoxide dismutase and glutathione peroxidase). An increased uptake of alpha-[3H]tocopherol (150% of controls) was observed in peripheral nerve of deficient animals from 11 weeks, whereas similar increases were not found in brain and cord until 36 weeks. These results were correlated with tests of neurological function which included electrophysiological studies and measurement of axonal transport. Recordings of somatosensory evoked potentials showed a significant delay (P less than 0.001) of central conduction velocity after 40 weeks of deficiency, whereas peripheral conduction was unchanged. After 40 weeks of deficiency, abnormal electromyographic activity of the hind limbs was obtained which was suggestive of chronic partial denervation. By 52 weeks there were significant reductions of both fast anterograde (P less than 0.02) and retrograde (P less than 0.05) transport of acetylcholinesterase in the deficient rats.
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PMID:Longitudinal studies of the neurobiology of vitamin E and other antioxidant systems, and neurological function in the vitamin E deficient rat. 246 31

The effects of Huperzine A (HupA), a novel acetylcholinesterase inhibitor, on hydrogen peroxide (H2O2) induced cell lesion, level of lipid peroxidation and antioxidant enzyme activities were investigated in rat pheochromocytoma line PC12. Following a 6-h exposure of the cells to H2O2 (200 microM), a marked reduction in cell survival and activities of glutathione peroxidase and catalase, as well as increased production of malondialdehyde (MDA) were observed. Pretreatment of the cells with HupA (0.1-10.0 microM) prior to H2O2 exposure significantly elevated the cell survival and antioxidant enzyme activities and decreased the level of MDA. Our results indicated that in addition to its anticholinesterase effects, HupA had protective effects against free radical-induced cell toxicity, which might be beneficial for the treatment of Alzheimer's disease.
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PMID:Huperzine A protects rat pheochromocytoma cells against hydrogen peroxide-induced injury. 1056 2

The effects of huperzine A (HupA), a novel acetylcholinesterase inhibitor, on Abeta(25-35)-induced cell lesion, level of lipid peroxidation, antioxidant enzyme activities were investigated in the rat pheochromocytoma line PC12. Following a 48 h exposure of the cells to Abeta(25-35), a significant reduction in cell survival and activities of glutathione peroxidase (GSH-Px) and catalase (CAT), as well as increased production of malondialdehyde (MDA) and superoxide dismutase (SOD) were observed. Preincubation of the cells with HupA prior to Abeta(25-35) exposure elevated the cell survival and GSH-Px and CAT activities, and decreased the level of MDA and SOD activity. The results indicate that HupA has protective effects against Abeta-induced cell toxicity, which might be beneficial for the treatment of Alzheimer's disease.
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PMID:Protective effects of huperzine A on beta-amyloid(25-35) induced oxidative injury in rat pheochromocytoma cells. 1083 8

Increased oxidative stress resulting from free radical damage to cellular function is associated with a number of neurodegenerative diseases, in particular with Alzheimer's disease (AD). The deposition of amyloid beta-peptide (Abeta), the major pathological hallmark for AD, has been suggested as the central disease-causing and disease-promoting event for the disease, and the pathological role of Abeta was partially mediated by oxidative stress. Here we compared the effects of huperzine A (HupA) and tacrine, two acetylcholinesterase (AChE) inhibitors available for AD, on Abeta-induced cell lesion, level of lipid peroxidation, and antioxidant enzyme activities in rat PC12 and primary cultured cortical neurons. Following exposure of both cells to different concentrations of an active fragment of Abeta, a marked reduction in cell survival and activities of glutathione peroxidase (GSH-Px) and catalase (CAT), as well as increased production of malondialdehyde (MDA) and superoxide dismutase (SOD), were observed. Pretreatment of the cells with HupA or tacrine (0.1-10 microM) prior to Abeta exposure significantly elevated the cell survival and GSH-Px and CAT activities and decreased the level of MDA. Both drugs have similar protection against Abeta insult. Our results indicate that HupA and tacrine exert neuroprotective effects against Abeta toxicity, which might be of importance and might contribute to their clinical efficacy for the treatment of AD.
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PMID:Huperzine A and tacrine attenuate beta-amyloid peptide-induced oxidative injury. 1095 26

A number of studies indicate that free radicals are involved in the neurodegeneration in Alzheimer's disease (AD). The present study was mainly conducted to examine the effect of Huperzine B on H(2)O(2) induced toxicity in rat pheochromocytoma line PC12 by measuring cell lesion, level of lipid peroxidation and antioxidant enzyme activities. Following a 30 min exposure of the cells to H(2)O(2) (150 microM), a marked decrease in cell survival, activities of glutathione peroxidase and catalase as well as increased production of malondialdehyde (MDA) were found. Pretreatment of the cells with huperzine B (10-100 microM) prior to H(2)O(2) exposure significantly elevated the cell survival, antioxidant enzyme activities and decreased the level of MDA. The above-mentioned neuroprotective effects are also observed with tacrine (1 microM), donepezil (10 microM) and galanthamine (10 microM), suggesting that the neuroprotective effects of cholinesterase inhibitor might partly contribute to the clinical efficacy in AD treatment.
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PMID:Huperzine B, a novel acetylcholinesterase inhibitor, attenuates hydrogen peroxide induced injury in PC12 cells. 1099 45

We have previously demonstrated that the loss of glutathione (GSH) and GSH-peroxidase (GSH-PX) in banked red blood cells (RBCs) is accompanied by oxidative modifications of lipids, proteins and loss of membrane integrity. The objective of this study was to determine whether artificial increases in antioxidant (GSH) or antioxidant enzyme (catalase) content could protect membrane damage in the banked RBCs following an oxidant challenge. RBCs stored at 1-6 degrees C for 0, 42 and 84 days in a conventional additive solution (Adsol) were subjected to oxidative stress using ferric/ascorbic acid (Fe/ASC) before and after enriching them with GSH or catalase using a hypotonic lysis-isoosmotic resealing procedure. This lysis-resealing procedure in the presence of GSH/catalase raised intracellular GSH and catalase concentrations 4-6 fold, yet produced only a small reduction in mean cell volume (MCV), mean cell hemoglobin (MCH) and mean cell hemoglobin concentrations (MCHC). Indicators of oxidative stress and membrane integrity were measured, including acetylcholinesterase (AChE) activity, GSH concentration, phosphatidylserine (PS) externalization (prothrombin-converting activity) and transmembrane lipid movements (14C-lyso phosphatidylcholine flip-flop and PS transport). GSH-enrichment protected AChE activity in fresh (0 day) and stored (42 and 84 days) RBCs from Fe/ASC oxidation by 10, 23 and 26%, respectively, compared with not-enriched controls. Following oxidative stress, the rate of transbilayer lipid flip-flop did not increase in fresh cells, but increased 9.3% in 42-day stored cells. Phosphatidylserine exposure, as measured by prothrombinase activity, increased 2.4-fold in fresh and 5.2-fold in 42-day stored cells exposed to Fe/ASC. Previous studies have shown that 42-day storage causes a moderate decrease in PS transport (approximately 50%), whereas transport rates declined by up to 75% in stored RBCs when challenged with Fe/ASC. GSH-enrichment prevented the increase in passive lipid flip-flop and the increase in prothrombinase activity, but offered no protection against oxidative damage of PS transport. In contrast to these effects, catalase-enrichment failed to protect GSH levels and AChE activity upon oxidative stress. Membrane protein thiol oxidation was assessed by labeling reactive protein thiols with 5-acetalamidofluorescein followed by immunoblotting with antifluorescein antibodies. Significant oxidation of membrane proteins was confirmed by a greater loss of thiols in stored RBCs than in fresh RBCs. These results demonstrate that it may be possible to prevent storage-mediated loss of AChE, increased lipid flip-flop, and increased PS exposure, by maintaining or increasing GSH levels of banked RBCs.
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PMID:Glutathione loading prevents free radical injury in red blood cells after storage. 1120 85

A number of studies indicate that free radicals are involved in the neurodegeneration in Alzheimer's disease (AD). The role of superoxide anion (O2*-) in neuronal cell injury induced by reactive oxygen species (ROS) was examined in PC12 cells using pyrogallol (1,2,3-benzenetrior), a donor to release O2*-. Pyrogallol induced PC12 cell death at concentrations, which evidently increased intracellular O2*-, as assessed by O2*- sensitive fluorescent precursor hydroethidine (HEt). A water extract of Curcuma longa L. (Zingiberaceae) (CLE), having O2*- scavenging activity rescued PC12 cells from pyrogallol-induced cell death. Hypoxia/reoxygenation injury of PC12 cells was also blocked by CLE. The present study was also conducted to examine the effect of CLE on H2O2 -induced toxicity in rat pheochromocytoma line PC12 by measuring cell lesion, level of lipid peroxidation and antioxidant enzyme activities. Following a 30 min exposure of the cells to H2O2 (150 microM), a marked decrease in cell survival, activities of glutathione peroxidase and catalase as well as increased production of malondialdehyde (MDA) were found. Pretreatment of the cells with CLE (0.5-10 microg/ml) prior to H2O2 exposure significantly elevated the cell survival, antioxidant enzyme activities and decreased the level of MDA. The above-mentioned neuroprotective effects are also observed with tacrine (THA, 1 microM), suggesting that the neuroprotective effects of cholinesterase inhibitor might partly contribute to the clinical efficacy in AD treatment. Further understanding of the underlying mechanism of the protective effects of these radical scavengers reducing intracellular O2*- on neuronal cell death may lead to development of new therapeutic treatments for hypoxic/ischemic brain injury.
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PMID:A water extract of Curcuma longa L. (Zingiberaceae) rescues PC12 cell death caused by pyrogallol or hypoxia/reoxygenation and attenuates hydrogen peroxide induced injury in PC12 cells. 1535 Aug 33

In the present work we investigated the effect of ovariectomy on Na+, K+-ATPase and acetylcholinesterase (AChE) activities in rat hippocampus. We also studied some parameters of oxidative stress, namely total radical-trapping antioxidant potential (TRAP), thiobarbituric acid-reactive substances (TBA-RS), as well as the antioxidant enzyme activities superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities. Our hypothesis is that ovariectomy might cause alterations in essential enzyme activities necessary to brain normal functioning and that these chances could be caused by oxidative stress. Female adult Wistar rats were divided into three groups: (1) naive (control); (2) sham-operated; and (3) ovariectomized. Thirty days after ovariectomy rats were sacrificed. Results showed that rats subjected to ovariectomy presented a significant increase in Na+, K+-ATPase, AChE and CAT activities, but did not change the oxidative stress parameters studied when compared to sham or naive rats. Since ovariectomy mimics postmenopausal changes, our findings showing alteration in the activities of brain Na+, K+-ATPase, AChE and CAT may be related to problems in postmenopausal women.
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PMID:Ovariectomy increases Na+, K+-ATPase, acetylcholinesterase and catalase in rat hippocampus. 1586 39

Effects of different herbicides on acetylcholinesterase (AChE), catalase and TBARS formation in teleost fish (Leporinus obtusidens) were studied. Fish were exposed during 30 days at concentrations of herbicides used in rice field. AChE activity in the brain decreased significantly after exposure to the herbicides clomazone and quinclorac. However, AChE activity increased significantly in muscle tissue after exposure to clomazone, propanil and metsulfuron methyl. Fish exposed to quinclorac, propanil and metsulfuron methyl showed TBARS decreased levels in brain and muscle tissues. However, TBARS and catalase activity increased in liver tissue after clomazone and propanil exposure. This study pointed out long-term effects on AChE activity, oxidative stress and antioxidant enzyme catalase in tissues of L. obtusidens after exposure to environmentally relevant concentrations of rice field herbicides. These parameters have been used to monitor fish toxicity in rice field system.
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PMID:Effects of four rice herbicides on some metabolic and toxicology parameters of teleost fish (Leporinus obtusidens). 1745 83

Polybrominated diphenyl ethers (PBDEs) are chemicals of environmental concern due to their lipophilic, persistent and bioaccumulable characteristics as well as for their potential endocrine disrupting role. Former studies carried out in a tributary of the Cinca river (Ebro basin, NE Spain) revealed high levels of PBDEs in fish due to the discharges of effluents rich in PBDEs coming from a nearby industrial park in Barbastro. In this study, several biomarkers of pollutants exposure were measured in barbel, Barbus graellsii, before (upstream) and after (downstream) the main industrial site (Barbastro) in the Vero river. The results evidenced an enhanced hepatic phase I and II metabolism (measured as reductases, glutathione S transferase and uridinediphospho-glucuronosyltransferase), and of the antioxidant enzyme glutathione peroxidase. Conversely, fishes collected from downstream reaches had their phase I CYP1A dependent ethoxyresorufin O-deethylase, antioxidant diaphorase and brain cholinesterase activities depleted. In addition, the histological study of the liver and kidney of these fish evidenced an increase of the number and size of macrophage aggregates in most individuals collected downstream. Bivariate correlated analyses showed that the above mentioned biomarkers were correlated to measured PBDE congeners, thus indicating that the observed biological effects were unlikely to be related to other environmental factors than PBDEs. Overall, the measured biochemical and histological markers provide new evidence that in field exposed fish, PBDEs levels were associated with high activities of phase I and II metabolic enzymes, oxidative stress in liver, neurotoxicity in brain and histopathological effects in both liver and kidney.
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PMID:First evidence of polybrominated diphenyl ether (flame retardants) effects in feral barbel from the Ebro River basin (NE, Spain). 1859 16


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