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)

Iron accelerates the production of reactive oxygen species (ROS). Excessive levels of ROS are thought to accelerate skeletal muscle fatigue and contribute to the loss of skeletal muscle mass and function with age. Patients with an iron overload disease frequently report symptoms of weakness and fatigue, which is attributed to reduced cardiac function. The contribution of skeletal muscle to these symptoms is unknown. Using a mouse model of iron overload, we determined the extent of iron accumulation in skeletal muscle and the concentrations of the iron storage protein ferritin. The level of oxidative stress, changes in antioxidant enzymes and exercise performance were also assessed. Compared with control mice, the iron overloaded mice had elevated levels of iron in the tibialis anterior muscle and a fourfold increase in ferritin light chain. The oxidative stress product malondialdehyde was increased in the iron group compared with the control group, as was the antioxidant enzyme activity of glutathione reductase and glutathione peroxidase. The iron group performed less work on an endurance test and produced less force in a strength test. Body weight and skeletal muscle weight were lower in the iron group following the intervention. Iron loading reduced the weight of the fast-twitch extensor digitorum longus muscle more than the slow-twitch soleus muscle. In summary, iron accumulation in skeletal muscle may play a significant role in the reduced exercise capacity seen in iron overload disorders and in ageing, and may play an underlying role in skeletal muscle atrophy.
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PMID:Iron injections in mice increase skeletal muscle iron content, induce oxidative stress and reduce exercise performance. 1920 85

Lakes receiving effluent from the Key Lake uranium mill in northern Saskatchewan contain elevated trace metals, some of which are associated with increased reactive oxygen species (ROS) in cells and tissues causing oxidative stress. The potential for oxidative stress was assessed in juvenile (age 1+) northern pike (Esox lucius) collected from two exposure (high and low) and one reference lake near the Key Lake operation. The concentrations of total, reduced and oxidized glutathione and the ratio of oxidized to reduced glutathione in liver and kidney did not differ significantly among pike collected from exposure and reference lakes, with the exception of low exposure pike kidney that had significantly greater oxidized glutathione and ratio of oxidized to reduced glutathione. The concentrations of by-products of lipid peroxidation (malondialdehyde and 4-hydroxyalkenal) were significantly greater in kidney of pike collected from the reference lake compared to both exposure lakes. The activity of the antioxidant enzyme glutathione peroxidase in liver was greater in pike collected from the high exposure lake compared to the reference lake. Histopathological evaluations revealed greater pathology in reference lake pike as indicated by a greater number of pyknotic and fragmented nuclei and dilated tubules as well as a thickening of Bowman's capsule in kidney, and as a thickening of the primary filament epithelial padding in gills. In liver, hepatocyte morphology, including transsectional area and degree of vacuolation, differed among lakes without any clear signs of pathology. Trace metal analyses of muscle showed that eight elements (arsenic, cobalt, copper, iron, molybdenum, selenium, thallium, and uranium) were significantly elevated in pike collected from both exposure lakes compared to reference. These results provide only limited evidence of oxidative stress in exposure pike tissues and no evidence of histopathology despite indications that trace metals, most notably arsenic and selenium, were bioaccumulating in tissue.
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PMID:Assessment of oxidative stress and histopathology in juvenile northern pike (Esox lucius) inhabiting lakes downstream of a uranium mill. 1930 30

In the current study, the effect of Ajuga iva extract on blood glucose, lipid profile, hepatic and renal toxicity and antioxidant enzyme activities in alloxan-induced diabetic rats was investigated. Diabetes was confirmed by measuring the glucoserua concentration 15 days after alloxan administration. Ajuga iva extract was administrated orally 3 weeks after alloxan injection. Our results investigate that Ajuga iva extract supplementation increased the levels of both enzymatic antioxidant (superoxide dismutase, catalase and glutathione peroxidase) and metals antioxidants (iron, copper, magnesium, calcium) and decreased lipid peroxidation level (TBARs). Besides Ajuga iva ameliorated diabetes provoked hepatic and renal toxicity appeared by a lower level in total and direct bilirubin, urea, creatinine, triglyceride (TG), cholesterol and a higher level in HDL-cholesterol. Besides, the activities of phosphatase alkalines (PAL), aspartate and lactate transaminase (AST & ALT) were decreased. The benefices effects of phytoecdysteroids of Ajuga iva confirmed by histological observation in pancreatic tissues. In conclusion, Ajuga iva phytoecdysteroids supplements seem to be beneficial for correcting the hyperglycemia and preventing diabetic complications in liver, pancreas and kidneys.
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PMID:Therapeutic effect of phytoecdysteroids rich extract from Ajuga iva on alloxan induced diabetic rats liver, kidney and pancreas. 1947 20

Iron sucrose (Venofer; reference) has a good safety record and is prescribed in patients with anaemia and chronic kidney disease worldwide, but various iron sucrose similar (ISS) preparations are now utilized in clinical practice. This study evaluates possible differences between iron sucrose and ISS preparations on haemodynamic and oxidative stress markers in normal rats. 60 male and 60 female Sprague Dawley rats were divided into four groups and assigned to receive commercially available ISS test 1, ISS test 2, reference or isotonic saline solution (control). A single i.v. dose of iron (40 mg/kg) or saline (equivalent volume) was administered after 24 h and every 7 days for 4 weeks. Blood samples were collected for biological assessment of haemoglobin (Hb), serum iron and percentage transferrin saturation (TSAT), and urine samples were collected to investigate creatinine clearance and proteinuria. Animals were sacrificed after receiving an i.v. dose on days 1, 7 and 28, and kidney, liver, and heart homogenates were then collected to determine antioxidant enzyme levels. Tissues were processed using Prussian blue and immmunohistochemistry techniques to identify iron deposits, tissue ferritin and pro-inflammatory markers. Systolic blood pressure was significantly reduced in the ISS groups relative to the reference and control groups after 24 h and on days 7, 14 and 21 (p < 0.05). Creatinine clearance was reduced (p < 0.01) and proteinuria marked (p < 0.01) in the ISS groups at 24 h and on days 7 and 28 relative to the reference and control groups which did not differ throughout the study. Liver enzymes were also increased in the ISS groups at 24 h and on days 7 and 28. Both ISS test 1 and ISS test 2 groups presented a significant increase in catalase, thiobarbituric reactive species, Cu, Zn-superoxide dismutase (CuZnSOD) and glutathione peroxidase activity, and a decrease in glutathione levels (p < 0.01) in the liver, heart and kidney at 24 h and on day 7 relative to the reference and control groups. Serum iron and percentage TSAT were elevated in all groups (except control) (p < 0.01) but no differences in Hb concentration were observed between them. Finally, levels of the proinflammatory markers TNF-alpha and IL6 were significantly elevated in the ISS groups (liver, heart and kidney) compared with the reference and control groups on day 28 (p < 0.01). These findings suggest significant differences between the reference and ISS test 1/ISS test 2 regarding oxidative stress and the inflammatory responses of liver, heart and kidneys in normal rats. A possible explanation for these observations could be the stability of the iron complex.
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PMID:Differences between original intravenous iron sucrose and iron sucrose similar preparations. 1951 94

Astaxanthin (ASX), a red carotenoid pigment with no pro-vitamin A activity, is a biological antioxidant that occurs naturally in a wide variety of plants, algae and seafoods. This study investigated whether ASX could inhibit glycated protein/iron chelate-induced toxicity in human umbilical-vein endothelial cells (HUVEC) by interfering with ROS generation in these cells. Glycated fetal bovine serum (GFBS) was prepared by incubating fetal bovine serum (FBS) with high-concentration glucose. Stimulation of cultured HUVECs with 50 mm 1 mL of GFBS significantly enhanced lipid peroxidation and decreased antioxidant enzyme activities and levels of phase II enzymes. However, preincubation of the cultures with ASX resulted in a marked decrease in the level of lipid peroxide (LPO) and an increase in the levels of antioxidant enzymes in an ASX concentration-dependent manner. These results demonstrate that ASX could inhibit LPO formation and enhance the antioxidant enzyme status in GFBS/iron chelate-exposed endothelial cells by suppressing ROS generation, thereby limiting the effects of the AGE-RAGE interaction. The results indicate that ASX could have a beneficial role against glycated protein/iron chelate-induced toxicity by preventing lipid and protein oxidation and increasing the activity of antioxidant enzymes.
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PMID:Cytoprotective role of astaxanthin against glycated protein/iron chelate-induced toxicity in human umbilical vein endothelial cells. 1954 80

The divalent cations of several transition metal elements have similar chemical properties and, when present in excess, one metal can interfere with the homeostasis of another. To better understand the role of interactions between transition metals in the development of metal toxicity symptoms in plants, the effects of exposure to excess nickel (Ni) on copper (Cu) and iron (Fe) homeostasis in the Ni hyperaccumulator plant Alyssum inflatum were examined. Alyssum inflatum was hypertolerant to Ni, but not to Cu. Exposure to elevated subtoxic Ni concentrations increased Cu sensitivity, associated with enhanced Cu accumulation and enhanced root surface Cu(II)-specific reductase activity. Exposure to elevated Ni concentrations resulted in an inhibition of root-to-shoot translocation of Fe and concentration-dependent progressive Fe accumulation in root pericycle, endodermis and cortex cells of the differentiation zone. Shoot Fe concentrations, chlorophyll concentrations and Fe-dependent antioxidant enzyme activities were decreased in Ni-exposed plants when compared with unexposed controls. Foliar Fe spraying or increased Fe supply to roots ameliorated the chlorosis observed under exposure to high Ni concentrations. These results suggest that Ni interferes with Cu regulation and that the disruption of root-to-shoot Fe translocation is a major cause of nickel toxicity symptoms in A. inflatum.
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PMID:Interference of nickel with copper and iron homeostasis contributes to metal toxicity symptoms in the nickel hyperaccumulator plant Alyssum inflatum. 1969 76

Oxidative stress is a key factor involved in the development and progression of Alzheimer disease (AD), and it is well documented that free radical oxidative damage, particularly of neuronal lipids, proteins, nucleic acids, and sugars, is extensive in brains of AD patients. The complex chemistry of peroxynitrite has been the subject of intense study and is now evident that there are two principal pathways for protein modification: the first one involves homolytic hydroxyl radical-like chemistry that results in protein-based carbonyls and the second involves electrophilic nitration of vulnerable side chains, in particular the electron-rich aromatic rings of Tyr and Trp. In the presence of buffering bicarbonate, peroxynitrite forms a CO(2) adduct, which augments its reactivity. Formation of 3-nitrotyrosine by this route has become the classical protein marker specifically for the presence of peroxynitrite. Protein-based carbonyls can be detected by two methods: (i) derivatization with 2,4-dinitrophenylhydrazine (DNPH) and detection of the protein-bound hydrazones using an enzyme-linked anti-2,4-dinitrophenyl antibody and (ii) derivatization with biotin-hydrazide and detection of the protein-bound acyl hydrazone with enzyme-linked avidin or streptavidin. Glycation of proteins by reducing sugars (Maillard reaction) results in a profile of time-dependent adduct evolution rendering susceptibility to oxidative elaboration. In addition, oxidative stress can result in oxidized sugar derivatives which can subsequently modify protein through a process known as glycoxidation. Of more general importance, oxidative stress results in lipid peroxidation and the production of a range of electrophilic and mostly bifunctional aldehydes that modify numerous proteins. The more important protein modifications are referred to as advanced glycation end products (AGEs) and advanced lipoxidation end products (ALEs). Protein modification can result in both non-cross-link and cross-link AGEs and ALEs, the latter arising from the potential bifunctional reactivity, such as that of the lipid-derived modifiers 4-hydroxy-2-nonenal (HNE) and malondialdehyde (MDA). Oxidative damage to nucleic acids results in base modification, substitutions, and deletions. Among the most common modifications, 8-hydroxyguanosine (8OHG) is considered a signature of oxidative damage to nucleic acid.Cells are not passive to increased oxygen radical production but rather upregulate protective responses. In neurodegenerative diseases, heme oxygenase-1 (HO-1) induction is coincident with the formation of neurofibrillary tangles. This enzyme that converts heme, a prooxidant, to biliverdin/bilirubin (antioxidants) and free iron has been considered an antioxidant enzyme. But seen in the context of arresting apoptosis, HO-1 and tau may play a role in maintaining the neurons free from the apoptotic signal (cytochrome c), since tau has strong iron-binding sites. Given the importance of iron as a catalyst for the generation of reactive oxygen species, changes in proteins associated with iron homeostasis can be used as an index of cellular responses. One such class of proteins is the iron regulatory proteins (IRPs) that respond to cellular iron concentrations by regulating the translation of proteins involved in iron uptake, storage, and utilization. Therefore, IRPs are considered to be the central control components of cellular iron concentration.
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PMID:Detection and localization of markers of oxidative stress by in situ methods: application in the study of Alzheimer disease. 2001 93

Lipopolysaccharide (LPS) is a glycolipid component of the cell wall of gram-negative bacteria inducing deleterious effects on several organs including the liver and eventually leading to septic shock and death. Endotoxemia-induced hepatotoxicity is characterized by disturbed intracellular redox balance, excessive reactive oxygen species (ROS) accumulation inducing DNA, proteins and membrane lipid damages. Resveratrol (trans-3,5,4' trihydroxystilbene) is a phytoalexin polyphenol exhibiting antioxidant and anti-inflammatory properties. In this study, we investigated the effect of subacute pre-treatment with this natural compound on LPS-induced hepatotoxicity in rat. Resveratrol counteracted LPS-induced lipoperoxidation and depletion of antioxidant enzyme activities as superoxide dismutase (SOD) and catalase (CAT) but slightly glutathione peroxidase (GPx) activity. The polyphenol also abrogated LPS-induced liver and plasma nitric oxide (NO) elevation and attenuated endotoxemia-induced hepatic tissue injury. Importantly resveratrol treatment abolished LPS-induced iron sequestration from plasma to liver compartment. Our data suggest that resveratrol is capable of alleviating LPS-induced hepatotoxicity and that its mode of action may involve differential iron compartmentalization via iron shuttling proteins.
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PMID:Resveratrol, a red wine polyphenol, attenuates lipopolysaccharide-induced oxidative stress in rat liver. 2008 5

Dyslipidemia in patients with glycogen storage disease types Ia (GSD Ia) and III (GSD III) does not lead to premature atherosclerosis. The aim of this study was to investigate the association among serum copper (Cu), zinc (Zn), iron (Fe), and selenium (Se) concentrations, and their carrier proteins: ceruloplasmin, albumin, and related antioxidant enzyme activities [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), paraoxonase (PON), and arylesterase (ARYL)] in 20 GSD Ia and 14 III patients compared to age and sex matched 20 healthy subjects. Erythrocyte oxidative stress was measured by erythrocyte thiobarbituric acid reactive substances (eTBARSs). Hypertriglyceridemia [333 (36-890)mg/dL] in GSD Ia and hypercholesterolemia with elevated LDL-cholesterol [188 (91-313)mg/dL] and decreased HDL-cholesterol [32(23-58)mg/dL] levels in GSD III were found. Serum Cu, Fe, and Zn showed no significant differences between groups. However, Se 60 (54-94), 81 (57-127) microg/L, ceruloplasmin 21 (10-90), 27 (23-65) microg/L, and albumin 2.4 (1.7-5.1), 2.8 (1.8-4.06)g/dL levels were decreased in GSD Ia and III groups, respectively, in comparison with the controls [Se 110 (60-136) microg/L, ceruloplasmin 72 (32-94) microg/L, and albumin 4.4 (4-4.8)g/dL)]. In spite of high oxidative stress in erythrocyte detected by elevated eTBARS/Hb levels in GSD group [674.8 (454.6-948.2) for GSD Ia, 636.3 (460.9-842.1) for GSD III, and 525.6 (449.2-612.6)], the activities of CAT, SOD, ARYL, and PON in GSD patients were not different from the controls. GPx activity was decreased in GSD Ia [3.7 (1.8-7.1)U/mL] and GSD III [4.2 (2.2-8.6)U/mL] compared with healthy controls [7.1 (2.9-16.2)U/mL]. In conclusion, this study supplied the data for trace elements, their carrier, and antioxidative enzymes in the patients with GSD Ia and III. The trace elements and anti-oxidative enzyme levels in GSD patients failed to explain the atherosclerotic escape phenomenon reported in these patients.
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PMID:An association among iron, copper, zinc, and selenium, and antioxidative status in dyslipidemic pediatric patients with glycogen storage disease types IA and III. 2012 79

Oxidative stress-induced mitochondrial dysfunction is a common consequence of severe sepsis. However, oxidative stress also activates signalling cascades which enable protection of cells against subsequent oxidative damage. This study hypothesized that cellular uptake of vitamin C as dehydroascorbic acid rather than ascorbic acid would up-regulate antioxidant enzyme systems and impart a protective effect to mitochondria in cells subsequently exposed to lipopolysaccharide (LPS) in an iron free environment. Treatment of monocytes with dehydroascorbic acid, but not ascorbic acid, caused oxidative stress (p< 0.001). Dehydroascorbic acid exposure also resulted in increased manganese superoxide dismutase (p= 0.018) and catalase (p= 0.003) expression. Pre-treatment of monocytes with dehydroascorbic acid followed by LPS resulted in higher mitochondrial membrane potentials than cells without pre-treatment (p< 0.0001). Lower cytochrome c in cytosol (p< 0.05) and higher mitochondrial expression of the anti-apoptotic Bcl-2 protein (p= 0.029) was also found in monocytes pre-treated before subsequent LPS exposure, compared to cells without pre-treatment. In conclusion, acute exposure of monocytes to dehydroascorbic acid in an iron free environment induces cytoprotective antioxidant enzymes and protected mitochondria from the harmful effects of oxidative stress prior to a septic insult, which was abrogated when cells were pre-incubated with the DHA uptake inhibitor cytocholasin B.
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PMID:Dehydroascorbic acid as pre-conditioner: protection from lipopolysaccharide induced mitochondrial damage. 2016 93


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