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:1.15.1.1 (superoxide dismutase)
58,858 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Production of oxygen-free radicals has been proposed as one pathophysiologic mechanism for postburn cardiac contractile dysfunction in adults. To examine this hypothesis in young subjects, we studied the cardiac effects of polyethylene glycol-superoxide dismutase (PEG-SOD) and PEG-catalase (PEG-CAT), each given as 20 U/g of body weight with fluid resuscitation (Parkland formula), after a third-degree burn constituting 33% of the total body surface area in young (6- to 7-day old) guinea pigs (group 3, n = 12). Fluid-treated burns without scavenger therapy (group 2, n = 15) and sham burn controls (group 1, n = 15) were included. Animals were killed 24 hours postburn, and hearts were studied in vitro (Langendorff). Compared with sham burn controls, fluid-treated burns (group 2) had significant cardiac dysfunction as indicated by a lower peak systolic left ventricular (LV) pressure (LVP: 67 +/- 2 vs. 57 +/- 4 mm Hg, p = 0.01, mean +/- SEM), maximal rate of LV pressure development (+dP/dt max: 1169 +/- 45 vs. 988 +/- 45 mm Hg/second, p = 0.01), and fall (-dP/dt max: 1109 +/- 45 vs. 919 +/- 49 mm Hg/second, p = 0.01). In addition, LV function curves calculated for group 2 were shifted downward and to the right of those calculated for sham burn controls in the direction of contractile depression, p = 0.01. PEG-SOD/PEG-CAT treatment in burns did not significantly improve LVP (60 +/- 5 mm Hg), but scavenger therapy improved +/-dP/dt max values (1112 +/- 74 and 988 +/- 98 mm Hg/second, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of toxic oxygen metabolites in a young model of thermal injury. 747 25

We studied the effect of supplementation with vitamins C, E and beta-carotene (PARABION, produced by Syndipharma) on antioxidative status in kidneys of male Wistar rats with diabetes induced by intravenous application of streptozotocin (45 mg.kg-1 of body weight). The animals received subtherapeutic doses of Insulin Interdep (6 U.kg-1 of body weight). A significant decrease of malondialdehyde (MDA), reduced (GSH) and oxidized (GSSG) glutathione and reduction of the activities of Se-glutathione peroxidase (Se-GSH-PX, EC. 1.11.1.9.) and glutathione S-transferase (GST, EC. 2.5.1.18.) were observed in kidneys of diabetic rats treated with these vitamins. On the contrary, the activity of CuZn-superoxide dismutase (CuZn-SOD, EC. 1.15.1.1) and the level of vitamin C (vit. C) increased significantly. No changes were observed for vitamin E (vit. E), beta-carotene and catalase (CAT, EC. 1.11.1.6). Supplementation with vitamins C, E and beta-carotene resulted in an improvement of antioxidative status of kidneys of rats with streptozotocin-induced diabetes.
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PMID:Effect of intake of exogenous vitamins C, E and beta-carotene on the antioxidative status in kidneys of rats with streptozotocin-induced diabetes. 747 41

This investigation elucidates the role of antioxidant system in cisplatin induced nephrotoxicity and the nephroprotection with diethyldithiocarbamate (DDTC). Male Wistar rats were injected with 1) cisplatin; 2) cisplatin+DDTC and 3) vehicle control. Rats were sacrificed three days post-treatment and the corticomedullary junction of the kidney was isolated adn were analyzed for GSH, GSSG, SOD, CAT, and GSH.Px. Serum creatinine increased (500% of control) following cisplatin administration which decreased to 200% of control with DDTC. Cisplatin treated rats showed depletion of GSH levels, while cisplatin+DDTC injected rats had GSH values similar to controls. SOD and GSH.Px activities were found to be 63 and 40% of control following cisplatin administration which increased to 109 and 75% of control with DDTC respectively. Our findings suggest that cisplatin nephrotoxicity is mediated by impaired activities of SOD and GSH-Px enzymes and by GSH depletion. The protective mechanism of DDTC against cisplatin nephrotoxicity is related to the prevention of GSH depletion and restoring SOD and GSH-Px activities in the kidney of rats.
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PMID:Diethyldithiocarbamate protection against cisplatin nephrotoxicity: antioxidant system. 749 9

This investigation was undertaken to explain the possible, mechanism(s) of protection by diethyldithiocarbamate (DDTC) against cisplatin ototoxicity. Male Wistar rats (250-275 g) underwent pretreatment auditory brain stem-evoked responses (ABRs). The different groups of rats were injected as follows: (1) cisplatin (16 mg/kg i.p.), (2) cisplatin plus DDTC (16 mg/kg i.p. + 600 mg/kg, s.c.), and (3) control rats. Post-treatment ABRs were performed after 3 days and the rats were euthanized and cochleae were harvested. The cochleae were analyzed for glutathione (GSH) and oxidized glutathione, by HPLC, and for the activities of the antioxidant enzymes, and malondialdehyde levels, by spectrophotometry. The cisplatin-injected rats showed a threshold elevation of 36 +/- 3.05 dB above the pretreatment thresholds using click stimulus. Rats treated with cisplatin and then DDTC did not show a significant elevation of hearing threshold. DDTC-mediated protection was associated with higher levels of GSH (0.81 +/- 0.11 nmol/mg tissue), compared to 0.45 +/- 0.02 nmol/mg tissue following administration of cisplatin alone. Administration of cisplatin + DDTC restored the cochlear GSH-Px activity to control level. Cisplatin-treated rats were found to have decreased GSH-Px activity (75% of control). Cochlear SOD and CAT activities and MDA levels showed a decreasing trend in the animals injected with cisplatin + DDTC, compared to cisplatin-alone-treated rats. These data suggest that the protection conferred by DDTC against cisplatin ototoxicity is associated with sparing of the cochlear GSH/GSH-Px.
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PMID:Mechanism of protection by diethyldithiocarbamate against cisplatin ototoxicity: antioxidant system. 758 18

The ability of beta-carotene to protect against oxidative stress in vitro was assessed. Primary cultures of chicken embryo fibroblasts (CEF) were oxidatively stressed by exposure to paraquat (PQ). Activities of the antioxidant enzymes superoxide dismutase (SOD; EC 1.15.1.1), catalase (CAT; EC 1.11.1.6) and glutathione peroxidase (GSH-Px; EC 1.11.19) were measured as indices of oxidative stress. CEF incubated with 0.25 mM-PQ for 18 h exhibited increased SOD and CAT activities and decreased GSH-Px activity compared with the control (P < 0.001). Incorporation of added beta-carotene (0.1 microM) into 0.25 mM-PQ-treated CEF returned SOD activity to that seen in non-PQ-treated cells. beta-Carotene (0.1 microM) reduced the CAT activity from that seen in PQ-treated cells and returned the GSH-Px activity to its control value thus protecting the cells against PQ-induced oxidative stress. However, at higher concentrations of beta-carotene (10 microM), SOD and CAT activities increased significantly (P < 0.001) relative to non-PQ-treated cells and GSH-Px activity decreased relative to its control value. Similar trends were observed when CEF grown in beta-carotene-enriched media (0.1-10 microM) were oxidatively stressed by exposure to 0.25 mM-PQ for 18 h.
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PMID:Modulation of oxidative stress by beta-carotene in chicken embryo fibroblasts. 763 65

Lipoprotein abnormalities are a risk factor for atherosclerotic disease and considered to accelerate glomerular injury in kidney disease. Serum levels of Lp(a) are elevated in patients with nephrotic syndrome and Lp(a) deposits are found in diseased glomeruli. Since mesangial hypercellularity is a prominent feature in a variety of glomerular diseases, we studied the effects of Lp(a) on proliferation of cultured rat mesangial cells. DNA synthesis was stimulated in cells incubated in the presence of Lp(a) as were the mRNA levels for c-fos and c-myc, two "early genes" that serve as transcription factors. Lp(a) also accelerated cell growth by 42 +/- 6% compared to control cells. Increased DNA synthesis was partially blunted, when cells were incubated with Lp(a) in the presence of oxygen radical scavengers CAT and SOD. We conclude that Lp(a) abnormalities are likely to contribute to glomerular injury in kidney disease. The mechanism by which Lp(a) alters the proliferation rate of mesangial cells involves the formation of reactive oxygen species.
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PMID:[Atherogenic lipoprotein(a) as a progression factor in glomerular diseases: studies in cultured rat mesangial cells]. 774 26

Aerobic cells have several scavenger systems for protection from reactive oxygen species (ROS). We developed an ROS-resistant variant of the human erythroleukemic cell line K562 by culturing cells in glucose oxidase to produce hydrogen peroxide. Testing the activity of the scavenger systems for ROS showed these cells had a 25- to 28-fold increase in catalase activity. We therefore termed this variant cell line K562-CAT. There was no similar increase in glutathione content or activity of superoxide dismutase and glutathione peroxidase. To determine what effect the increased catalase activity would have on the immune response to these tumor cells, we compared K562 and K562-CAT sensitivity to tumor necrosis factor-alpha (TNF alpha) activated polymorphonuclear neutrophil (PMN), natural killer (NK), and lymphokine-activated killer (LAK) cells. K562-CAT showed a significant increase in resistance to TNF alpha-activated PMN but not to NK or LAK, confirming the role of ROS in the former but not the latter. We also tested K562-CAT sensitivity to cisplatin and mitomycin C, agents known to involve ROS in their cytotoxic mechanism. There was no increased resistance in K562-CAT compared to parental K562, indicating that catalase is not involved in tumor cell resistance to those drugs. Given the characteristics of its resistance to the immune response, K562-CAT or a similar catalase-hyperexpressing cell line could be useful in determining the significance of TNF alpha-activated PMN in antitumor defenses.
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PMID:Characterization of an oxidation-resistant tumor cell line and its sensitivity to immune response and chemotherapy. 774 66

We examined the role of reactive oxygen metabolites and the protective effect of zinc-induced metallothionein (MT) synthesis on gentamicin nephrotoxicity both in vivo and in vitro. In vivo study we found that the MT content of renal cortex of the zinc preinjected rats was significantly increased, and proximal tubular necrosis and acute renal failure caused by injection of gentamicin were ameliorated. In suspended proximal tubules (PT), Na(+)-K(+)-ATPase activity and DNA synthesis were suppressed by the addition of gentamicin, but in zinc-pretreated rats' PT, these were not suppressed by the addition of gentamicin. Meanwhile MDA and hydroxyl radicals were significantly less in zinc-pretreated rats' PT compared to that in the control. Finally, we found that gentamicin enhanced superoxide anion and hydroxyl radical productin in renal cortical mitochondria. Superoxide anion could be suppressed by SOD and hydroxyl radical could be scavenged by DMSO, DFO and CAT. Our data confirm that hydroxyl radicals play a role in the pathogenesis of gentamicin nephrotoxicity, gentamicin can induce suppression of Na(+)-K(+)-ATPase activity and DNA synthesis in rats' proximal tubules leading to renal injury; this injury may be relevant to reactive oxygen metabolites generated by gentamicin. Renal cortical mitochondria is the source of reactive oxygen metabolites, which induces renal injury, and zinc-induced metallothionein synthesis could ameliorate gentamicin nephrotoxicity via scavenging reactive oxygen metabolites.
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PMID:Mechanism of gentamicin nephrotoxicity in rats and the protective effect of zinc-induced metallothionein synthesis. 780 Feb 47

We investigated the role of free radicals, especially from activated neutrophils, in acute xanthine and xanthine oxidase-induced lung injury in rats. We evaluated the effects of intravenously administered intracellular and extracellular free radical scavengers (for O2-., H2O2, and .OH), methylprednisolone (MP), and Ulinastatin (UST, a protease inhibitor), on this animal model of lung injury. At 5 min prior to the intrabronchial injection of a mixture of xanthine (X, 100 nmol) and xanthine oxidase (XO, 1 unit) used to induce unilateral lung damage, rats were pretreated intravenously with superoxide dismutase (SOD, 40 mg/kg), SOD (40 mg/kg) plus catalase (CAT, 30 mg/kg), dimethylthiourea (DMTU, 500 mg/kg), N-2-mercaptopropionyl glycine (MPG, 20 mg/kg), MP, 30 mg/kg, and UST, 50,000 units/kg. Each scavenger was infused intravenously at one-half the initial dose for 20 min after intrabronchial injection; 3 hr later, we examined the wet/dry lung weight ratios and the levels of thiobarbituric acid-reactive substances (TBARS) in lung tissue. Intrabronchial injection of the X/XO mixture markedly increased wet/dry lung weight ratios and lung tissue content of TBARS. Histopathologic changes were observed in the injected lung as well. Pretreatment with SOD + CAT, DMTU, and UST significantly reduced the increases in wet/dry lung weight ratios and lung tissue content of TBARS induced by the intrabronchial injection of the X/XO mixture. Our data suggest indirectly that free radicals (H2O2, .OH) and proteases from activated neutrophils may contribute, in part, to the lung damage induced by the O2-.-generating system of xanthine and xanthine oxidase.
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PMID:Effects of free radical scavengers, methylprednisolone, and ulinastatin on acute xanthine and xanthine oxidase-induced lung injury in rats. 783 23

The purpose of this study was to determine dismutase and catalase activities in erythrocytes of psoriatic patients with psoriasis vulgaris topically treated with an ointment (in accordance with recommendations of the Helsinki Declaration), in which 2-chloroethyl-3-chloropropyl sulfide (CLEPS) is an active compound. SOD activity in hemolysates was determined according to the method of Misra and Fridovich [12] and calculated as units per g of hemoglobin. CAT activity in hemolysates was determined by Beers and Sizer method [2] and expressed in U/g Hb. SOD activity in the control group was 1.61 +/- 0.48 U/g Hb x 10(3). However, the activity of CAT was 5.72 +/- 1.17 U/g Hb x 10(4). Before treatment SOD activity was decreased by ca. 22.5% (1.25 +/- 0.53 U/g Hb x 10(3)) while that of CAT by about 7% (5.30 +/- 1.41 U/g Hb x 10(4)), in comparison with the normal control. After treatment with the ointment, activity of both enzymes increased by about 18% to 1.55 x 10(3) U/g Hb and by about 16.5% to 6.25 x 10(4) U/g Hb, respectively. The results of our investigations showed that the ointment (containing mustard gas derivative) applied on psoriatic skin, causes increased of SOD and CAT activity in erythrocytes after regression of psoriatic lesions and treatment termination.
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PMID:Superoxide dismutase and catalase activity in psoriatic patients treated topically with ointment containing 2-chloroethyl-3-chloropropyl sulfide. 789 31


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