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)

Oxidative stress is involved in both the pathogenesis and complications of diabetes. ACE inhibitors can slow the progression of cardiac and renal impairments related to diabetes. The effect of enalapril treatment on oxidative stress and tissue injury was studied in hearts, kidneys, and livers from streptozotocin-induced diabetic rats. Twenty-four rats were divided into the following groups: streptozotocin (65 mg/kg, single intraperitoneal dose), streptozotocin+enalapril (20 mg enalapril/L drinking water), and control (intraperitoneal saline). Seven months after streptozotocin injection, organs were studied by light microscopy and collagen III immunolabeling. Tissue lesions and collagen labeling were graded by a semiquantitative score (0 to 4). Total glutathione content, glutathione redox status (reduced/oxidized glutathione), antioxidant enzyme activities, protein-associated sulfhydryls, thiobarbituric acid-reactive substances, and fluorescent chromolipids were determined in tissue homogenates. Glycemia was higher in both the streptozotocin and streptozotocin+enalapril groups relative to the control group. In the streptozotocin group, creatinine clearance and body weight were lower, and systolic blood pressure and urinary albumin excretion were higher than in the streptozotocin+enalapril and control groups. Heart, kidney, and liver lesion/labeling scores were significantly higher in the streptozotocin group compared with the streptozotocin+enalapril and control groups. Kidney and liver total glutathione was lower in the streptozotocin group relative to the control group (P<0.05). Enalapril treatment significantly attenuated the reduction of total glutathione. In the heart, kidney, and liver, both glutathione and proteins were relatively more oxidized in the streptozotocin group relative to the control group (P<0.05). Protein and glutathione oxidation were attenuated in the streptozotocin+enalapril group in the 3 tissues studied (P<0.05). Enalapril treatment attenuated the oxidation of lipids in the heart and kidney (P<0.05). Tissue fibrosis scores were inversely correlated with (1) both total glutathione and reduced/oxidized glutathione in heart, kidney, and liver and (2) glutathione reductase activity in the kidney. These results suggest that in streptozotocin-induced diabetic rats, the protective action of enalapril might be mediated, at least in part, by its effect on tissue oxidant/antioxidant status.
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PMID:Enalapril attenuates oxidative stress in diabetic rats. 1171 10

Biological aging is associated with increased cellular levels of reactive oxygen species (ROS) as well as the formation and accumulation of oxidized biomolecules. During evolution, organisms developed a highly-efficient and adaptive antioxidant defense system. Antioxidants can generally be divided into two categories: enzymatic and non-enzymatic. During the aging process the activity of antioxidant enzymes, e.g. SOD, CAT, GSH-Px, and GSSG-R, depends on factors such as race, gender, tissue and subcellular localization of enzymes. The age-dependent decrease in antioxidant enzyme activity may be attributed to oxidative modifications of enzymes. During the aging process, ROS may also lead to the induction of some enzyme activity which is explained as an adaptive phenomenon. The decrease in GSH concentration with age can be explained by decreased GSH synthesis and/or increased GSH consumption in the removal of peroxides and xenobiotics. In plasma albumin, ferritin, transferrin, and caeruloplasmin exert protective action. Plasma proteins can inhibit ROS generation and lipid peroxidation by chelating free transition metals. Plasma protein concentrations changes with age. The major exogenous antioxidants, mostly derived from the diet, are vitamin E, C, A, and beta-carotene. During the aging process the level of vitamins may decrease or increase, depending on such factors as diet, and diseases.
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PMID:[Antioxidative abilities during aging]. 1507 54

We report that albumin is translocated to the nucleus in response to oxidative stress. Prior measurements have demonstrated that in concert with known transcription factors albumin binds to an antioxidant response element, which controls the expression of glutathione S-transferase and other antioxidant enzymes that function to mediate adaptive cellular responses [Holderman, M. T., Miller, K. P., Dangott, L. J., and Ramos, K. S. (2002) Mol. Pharmacol. 61, 1174-1183]. To investigate the mechanisms underlying this adaptive cell response, we have identified linkages between calcium signaling and the nuclear translocation of albumin in JB6 epithelial cells. Under resting conditions, albumin and the calcium regulatory protein calmodulin (CaM) co-immunoprecipitate using antibodies against either protein, indicating a tight association. Calcium activation of CaM disrupts the association between CaM and albumin, suggesting that transient increases in cytosolic calcium levels function to mobilize intracellular albumin to facilitate its translocation into the nucleus. Likewise, nuclear translocation of albumin is induced by exposure of cells to hydrogen peroxide or a phorbol ester, indicating a functional linkage between reactive oxygen species, calcium, and PKC-signaling pathways. Inclusion of an antioxidant enzyme (i.e., superoxide dismutase) blocks nuclear translocation, suggesting that the oxidation of sensitive proteins functions to coordinate the adaptive cellular response. These results suggest that elevated calcium transients and associated increases in reactive oxygen species contribute to adaptive cellular responses through the mobilization and nuclear translocation of cellular albumin.
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PMID:Calmodulin involvement in stress-activated nuclear localization of albumin in JB6 epithelial cells. 1518 87

Many studies have shown the balance between the oxygen reactive species (ROS) and the antioxidant capacities, and that the massive ROS generation could lead to cell damage and diseases such as atherosclerosis, aging and cancer. Changes in antioxidant capacity like free radicals scavenging antioxidant agents such as vitamin E, C content, serum concentrations of bilirubin, uric acid, albumin and antioxidant enzyme systems like SOD, and GPx activities have been described to be related to many diseases. However, the research on chronic airway inflammatory disease and the antioxidant defence system is still not enough. Understanding of the antioxidant status and antioxidant enzymes in asthmatic patients is still unclear. In the present controlled study, we investigated the total antioxidant status (TAS) in serum and the antioxidant enzyme (total SOD and GPx) activities in 46 asthmatic children and 52 normal controls. The serum level of TAS in asthmatic children was significantly lower than the controls. The SOD concentration in asthmatic children was higher than the control, however the GPx was much lower than the control children, even though it was not statistical significance. In conclusion, these results suggested the existence of higher oxidative stress and reactive oxygen species (ROS) in asthmatic children, and that the antioxidant capacities in asthmatic children were altered. If the production of ROS was persistent, it would result in chronic inflammation and the imbalance of oxidative-reductive status in those patients.
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PMID:Evaluation of the serum antioxidant status in asthmatic children. 1562 67

In many diseases, including progressive renal disorders, tissue injury and pathological intracellular signaling events are dependent on oxidative stress. Glutathione peroxidase-1 (Gpx1) is an antioxidant enzyme that is highly expressed in the kidney and removes peroxides and peroxynitrite that can cause renal damage. Therefore, we examined whether this abundant renal antioxidant enzyme limits renal damage during the development of type 1 diabetic nephropathy. Wild-type (Gpx1+/+) and deficient (Gpx1-/-) mice were made diabetic by intraperitoneal injection of streptozotocin (100 mg/kg) on 2 consecutive days. Diabetic Gpx1+/+ and -/- mice with equivalent blood glucose levels (23 +/- 4 mM) were selected and examined after 4 mo of diabetes. Compared with normal mice, diabetic Gpx1+/+ and -/- mice had a two- to threefold increase in urine albumin excretion at 2 and 4 mo of diabetes. At 4 mo, diabetic Gpx1+/+ and -/- mice had equivalent levels of oxidative renal injury (increased kidney reactive oxygen species, kidney lipid peroxidation, urine isoprostanes, kidney deposition of advanced glycoxidation, and nitrosylation end products) and a similar degree of glomerular damage (hypertrophy, hypercellularity, sclerosis), tubular injury (apoptosis and vimentin expression), and renal fibrosis (myofibroblasts, collagen, TGF-beta excretion). A lack of Gpx1 was not compensated for by increased levels of catalase or other Gpx isoforms in diabetic kidneys. Contrary to expectations, this study showed that the high level of Gpx1 expressed in the kidney is not protective against the development of renal oxidative stress and nephropathy in a model of type 1 diabetes.
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PMID:Kidney expression of glutathione peroxidase-1 is not protective against streptozotocin-induced diabetic nephropathy. 1582 46

Changes in albumin and antioxidant enzyme mRNA expression in infant rat liver following administration of total parenteral nutrition (TPN) with/without soybean oil emulsion were studied. Infant rats were divided into three groups: group 1=oral diet, group 2=TPN without fat, and group 3=TPN with 20% of calories from soybean oil emulsion. The period of TPN administration was 4 d. Serum aspartate aminotransferase and alanine aminotransferase levels were higher in group 2 than in the other groups, with similar levels seen in the other groups. Albumin, Cu, Zn-superoxide dismutase, and glutaredoxin 1 mRNA expression levels were lower in group 2 than in the other groups, with similar levels seen in the other groups. Catalase mRNA expression was higher in group 1 than in the other groups, with the lowest level seen in group 2. Soybean oil emulsion should be included in TPN regimens to prevent down-regulation of albumin and antioxidant enzyme mRNA expression.
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PMID:Soybean oil in total parenteral nutrition maintains albumin and antioxidant enzyme mRNA levels. 1599 11

Inhaled cigarette smoke induces oxidative stress in the epithelium of airways. Peroxiredoxin V (PRXV) is a potent antioxidant protein, highly expressed in cells of the airway epithelium. The goal of our study was to determine whether cigarette smoke extract (CSE) influenced expression of this protein in airway epithelia in vivo and in vitro. In Sprague-Dawley rats, we determined effects of CSE on airway epithelial permeability, mRNA levels and expression of PRXV protein. Exposure of isolated tracheal segment in vitro to 20% CSE for 4 h resulted in development of increased permeability to albumin, significantly reduced mRNA levels for PRXV, and reduced amounts of PRXV protein in the epithelium. In cultures of the airway epithelial cell lines (Calu-3, JME), primary airway cell culture (cow), and alveolar epithelial cells A549, CSE also significantly decreased transepithelial electrical resistance and expression of PRXV protein, and induced glutathione and protein oxidation. To demonstrate functional importance of PRXV, we exposed clones of HeLa cells with siRNA-downregulated PRXV to hydrogen peroxide, which resulted in increased rate of cell death and protein oxidation. CSE directly downregulates expression of functionally important antioxidant enzyme PRXV in the epithelial cells of airways, which represents one pathophysiological mechanism of cigarette smoke toxicity.
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PMID:Cigarette smoke extract inhibits expression of peroxiredoxin V and increases airway epithelial permeability. 1632 4

In vitro studies have shown that activation of protein kinase C (PKC) is a key mediator of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) in a range of cell types and in response to high glucose, however, its role in the in vivo setting has not been clearly delineated. Streptozotocin-induced diabetic rats were treated with the PKC-beta isoform inhibitor LY333531 for 8 weeks. LY333531 treatment significantly attenuated increased urinary albumin excretion rate and glomerular volume and tubulointerstitial injury index as well as elevated PKC activity and PKC-beta protein expression in the kidney. Level of malondialdehyde was markedly higher and antioxidant enzyme activity such as superoxide diamutase and catalase as well as glutathione peroxidase were significantly lower in the kidney from diabetic rats than that of the control group. LY333531 administration could remit these changes. Increased macrophages recruitment as well as ICAM-1 and MCP-1 protein expression in the kidney were significantly inhibited by LY333531 in diabetic rats. It is concluded that mechanism of renoprotection of LY333531 may be correlated, at least partly, with suppression of increased macrophages recruitment and overexpression of ICAM-1 and MCP-1 in diabetic rats.
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PMID:Protein kinase C beta inhibitor LY333531 attenuates intercellular adhesion molecule-1 and monocyte chemotactic protein-1 expression in the kidney in diabetic rats. 1689 64

Stannous chloride (SnCl2) is a reducing chemical agent used in several man-made products. SnCl2 can generate reactive oxygen species (ROS). Therefore, the present study has been carried out to investigate the antioxidant action of l-ascorbic acid (AA) in minimizing SnCl2 toxicity on lipid peroxidation, antioxidant enzyme, and biochemical parameters in male New Zealand white rabbits. Animals were assigned to one of four treatment groups: 0mg AA and 0mg SnCl2/kg BW (control); 40 mg AA/kg BW; 20mg SnCl2/kg BW; 20mg SnCl2 plus 40 mg AA/kg BW. Rabbits were orally administered the respective doses every other day for 12 weeks. Results obtained showed that SnCl2 significantly (P<0.05) induced thiobarbituric acid-reactive substances (TBARS; the marker of lipid peroxidation) in plasma, while the activities of glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT), and the level of sulfhydryl groups (SH-group) were decreased (P<0.05) in blood plasma. Aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (AlP), acid phosphatase (AcP) and lactate dehydrogenase (LDH) activities were decreased (P<0.05). Stannous chloride significantly (P<0.05) increased the levels of plasma total lipid (TL), cholesterol, triglyceride (TG), low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL), glucose, urea and total bilirubin. On the other hand, the level of plasma high-density lipoprotein (HDL), total protein (TP), albumin (A) and globulin (G) were significantly (P<0.05) decreased. Ascorbic acid alone significantly decreased the levels of TBARS, lipids and urea, and increased the activities of GST, SOD and CAT, and the levels of SH-group and proteins. While the rest of the tested parameters were not affected. Also, the presence of AA with SnCl2 alleviated its harmful effects on most of the tested parameters. Therefore, the present results revealed that treatment with AA could minimize the toxic effects of stannous chloride.
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PMID:Study of the protective effect of ascorbic acid against the toxicity of stannous chloride on oxidative damage, antioxidant enzymes and biochemical parameters in rabbits. 1743 20

In recent years there has been increasing interest in the potential beneficial effects of probiotic bacteria, particularly concerning their immune-modulating effects. Considering the involvement of free radicals in immunological processes, we tried to verify and compare the effects of probiotic (Lactobacillus casei) and conventional yoghurt on antioxidant and oxidant parameters in plasma of humans. In this study female volunteers consumed 100 g/day of probiotic (n = 17) or conventional yoghurt (n = 16) for two weeks (T1-T2) and 200 g/day for another two weeks (T2-T3). A wash-out phase lasting two weeks followed. Total antioxidant capacity (TAC), albumin, and bilirubin were determined photometrically, uric acid was determined by enzymatic methods, and vitamin E, carotenoids, malondialdehyde (MDA), and conjugated dienes (CD) were measured using high-performance liquid chromatography (HPLC). In the period of continuous yoghurt intake (T1-T3), mean concentrations of the antioxidants vitamin E, lycopene, and zeaxanthin decreased significantly (p < 0.01) in the probiotic and in the control group. The average concentrations of lutein, beta-carotene, albumin, uric acid, and bilirubin decreased significantly (p < 0.05) in the probiotic group, only. These alterations led to a significant (p < 0.001) decrease of the average TAC values during the period T1-T3 in both tested groups. In the interval of daily yoghurt consumption (T1-T3) the mean plasma levels of oxidant parameters MDA and CD increased significantly in the probiotic (MDA: p < 0.01; CD: p < 0.001) and the control group (CD: p < 0.01). The average activity of the antioxidant enzyme superoxide dismutase (SOD) was quite constant throughout the study in both groups. The mean activities of GSH-Px and catalase decreased significantly (p < 0.001) in the probiotic group, only after consuming yoghurt daily for four weeks (T1-T3). Although several parameters changed significantly during the study, no significant differences were observed between both investigated groups. Therefore, the results indicate a possible influence of both probiotic and conventional yoghurt on the plasma levels of antioxidant and oxidant parameters.
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PMID:The effect of daily consumption of probiotic and conventional yoghurt on oxidant and anti-oxidant parameters in plasma of young healthy women. 1789 81


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