Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.15.1.1 (superoxide dismutase)
 58,858 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of acetaldehyde administration for 4 weeks on antioxidant protection systems was investigated in liver of rats. Liver SOD activity was decreased from control value 542.4 U/g of tissue to 411.2 U/g of tissue in experimental group (24% decrease). GSH-Px activity was practically unchanged and liver CAT activity was significantly decreased (35%). Sulfhydryl compounds in liver non-proteins following ACH treatment were decreased from 4.22 mumol/g of tissue in control group to 2.86 mumol/g of tissue (23%). Furthermore acetaldehyde treatment caused significant increase in MDA level in liver (78% increase).
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PMID:The diminution of liver glutathione content and changes in activities of antioxidant enzymes in long-term acetaldehyde poisoning. 128 37

This paper introduces the essential experiences concerning studies of burn metabolism and nutrition in our institute in the past five years. 1. Three new and practical animal models were developed for studying gastro-enteral nutrition in burns. 2. With indirect calorimetry, resting energy expenditure (REE) of 92 burn adult patients were measured and analyzed, and on the basis of which a new formula for calculating nutritional supplement in Chinese burn adults was proposed: kcal/day = 1,000 x M2 (body surface area) + 25 x % TBSA (total burn surface area). 3. Through experimental and clinical studies, it was found that antiouperoxide agents (such as SOD, CAT), tolbutamide, glutamine and Chinese herb decoction Sizunzituang all exhibited modulating effects on postburn metabolism and nutrition, e.g. decreasing catabolism, reducing negative nitrogen balance, stimulating secretion of insulin, enhancing tissue utilization of glucose, maintaining the mass of enteral mucosa and improving functions of viscerae. 4. A new less irritating, simple and easy-to-introduce nasal-enteral nutrition tube was devised, which could pass through the pylorus easily into the duodenum usually within 6hrs without using a stylet. It would be useful in the early postburn enteral nutrition supplementation.
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PMID:[A 5-year interval report on study of burn metabolism and nutrition]. 130 52

The levels of free radicals in the whole blood of the patients with cor pulmonale were determined using the method of electron spin resonance (ESR). The concentrations of serum SOD were determined using RIA. The concentrations of the MDA, vitamin E, selenium and the activities of the SeGSHPx, CAT of the patients were also measured using biochemical methods. The results showed that the level of free radical in the whole blood and serum MDA, SOD increase if compared with that of control group. The activities of SeGSH-Px, CAT and the concentration of vitamin E in serum of the patients are in lower level. These indicate that there is impairment in free radical metabolism of the patients.
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PMID:[Studies of free radical metabolism in patients with cor pulmonale]. 133 59

The effects of reactive oxygen species (ROS) on cultured rat mesangial cells were studied by measuring planar cell surface area (PCSA) after incubation with xanthine plus xanthine oxidase (XXO), in the presence of superoxide dismutase (SOD; 5 micrograms/ml) or catalase (CAT; 20 micrograms/ml), or after incubation with H2O2. Myosin light chain (MLC) phosphorylation was assessed in cells prelabeled with o-[32P]phosphoric acid and incubated with H2O2, after protein separation with sodium dodecyl sulfate-polyacrylamide gel electrophoresis. A possible intermediate role for platelet-activating factor (PAF) was analyzed by preincubation of the cells with a PAF antagonist BN 52021 (BN, 5 x 10(-5) M) and by measuring PAF-specific [3H]acetate incorporation and immunoassayable PAF. XXO significantly decreased PCSA (14%), an effect abolished by CAT but not by SOD. H2O2 induced a similar effect, in a dose-dependent and time-dependent manner. MLC phosphorylation increased by 81 +/- 15% after H2O2 incubation, and this effect was blocked by BN. BN also completely blocked the effect of H2O2 on PCSA. PAF-specific [3H]acetate incorporation increased in the presence of H2O2 (from 6,886 +/- 2,030 to 58,703 +/- 16,063 counts.min-1.mg-1) as well as the immunoassayable PAF production by cells (from 0.90 +/- 0.19 to 6.71 +/- 2.27 ng/mg). These results suggest that ROS, particularly H2O2, could modulate the surface area of mesangial cells, modifying the ultrafiltration coefficient, thus explaining the decrease in glomerular filtration rate in those pathological situations characterized by an increased ROS synthesis. PAF could be involved in the genesis of these effects.
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PMID:Effects of reactive oxygen species on cultured rat mesangial cells and isolated rat glomeruli. 141 75

SOD, CAT, GSH-Px, and sulfhydryl compounds MDA contents in liver of rats treated with heparegen for 7, 14, and 21 days after alcoholic liver injury have been investigated. After use of this drug, we found beneficial effects on GSH-Px activity, sulfhydryl compounds (total and nonprotein), and MDA content and a partially beneficial effect on SOD and CAT activities. These enzyme activities after 21 days of drug administration were restored. Furthermore, heparegen shortens the time necessary for the return of AIAT and GGTP to normal value. This enzymatic data are supported by histological studies in light microscopy.
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PMID:The effect of heparegen on antioxidant enzyme activities in ethanol-induced liver injury in rats. 141 65

1. The activity of antioxidant defense enzymes (SOD, CAT, GSH-Px and GST) was analysed during the autumn and winter in the ground squirrel adapted to 30 degrees C and subsequently exposed to cold for 6 and 24 hr. 2. The liver CAT activity as well as the IBAT CAT and GSH-Px activities differed between animals adapted to 30 degrees C, studied in autumn, and those studied in winter. 3. MnSOD activity in the liver was increased in autumn but decreased in winter after 6 hr cold exposure reaching the control level 24 hr later. Cold exposure induced a decrease in CAT activity (except after 24 hr cold exposure in winter) and an increase in GSH-Px activity. Lower GST activity was found after 24 hr exposure to cold in winter. 4. The IBAT SOD activity decreased under the influence of cold during both seasons with a tendency to return to the control level only in winter. Cold exposure produced a decrease in GST in both seasons and CAT activity in autumn. GSH-Px activity was increased in winter only. 5. The results indicate a seasonal dependence of the activity of antioxidant defence enzymes in the ground squirrel. Seasonal influence was evidenced in animals exposed to cold as well.
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PMID:Seasonal dependence of the activity of antioxidant defence enzymes in the ground squirrel (Citellus citellus): the effect of cold. 161 72

In this study, using electron spin resonance (ESR), we investigated the relation at the time of reperfusion between free radicals originating from the mitochondria of the canine myocardium and arrhythmias induced by reperfusion as well as the effect of radical scavengers on both. The left anterior descending artery was ligated just below the first diagonal branch and then reperfused for 10 minutes in 48 adult mongrel dogs. The dogs were divided into six groups consisting of: 1) control group administered no radical scavengers (n = 8), 2) SOD group (n = 6) receiving superoxide dismutase (15,000 U/kg), 3) SOD + CAT group (n = 6) receiving SOD (15,000 U/kg) and catalase (45,000 U/kg), 4) L-SOD group (n = 6) receiving liposomal-encapsulated SOD (30,000 U/kg), 5) CV-3611 (2-O-octadecylascorbic acid) group (n = 8) receiving CV-3611 (10 mg/kg), and 6) CoQ10 group (n = 6) receiving coenzyme Q10 (10 mg/kg). SOD, SOD + CAT, L-SOD, CV-3611, and CoQ10 were administered into the left atrium prior to reperfusion. The second lead of the electrocardiogram was continuously monitored during the experiment. The following results were obtained. 1) The relative intensity (RI) of the electron spin resonance signal of the mitochondria of the reperfused portion of the myocardium was smaller (p less than 0.025) in the SOD, SOD + CAT, L-SOD, CoQ10 groups (1.08 +/- 0.36, 0.92 +/- 0.19, 0.91 +/- 0.11, and 0.81 +/- 0.09, respectively) than in the control group (1.70 +/- 0.20).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of some radical scavengers on reperfusion-induced arrhythmias in the canine heart. 164 21

Low-density lipoproteins (LDL) oxidized by oxygen radicals (OR) are a potent atherogenic stimulus. Chemically modified LDL are internalized by macrophages via a specific cell surface receptor that was termed the scavenger receptor, and may induce foam cells transformation. A free radical is any chemical species that has an unpaired electron. This property renders it highly chemically reactive. When a radical reacts with a non radical another free radical is generated. This characteristic enables radicals to trigger chain reactions. Oxygen radicals are: superoxide anion (.O2-), hydroxyl radical (.OH) and hydrogen peroxide (H2O2). It is unknown whether LDL are modified via direct lipid oxidation by OR, or whether LDL are subsequently oxidized via chain reactions after initial OR attack. To distinguish between these 2 mechanisms, LDL were exposed to OR formed by xanthine/xanthine oxidase (X/XO). Peroxidation was measured from malonyldialdehyde (MDA) levels. Parallel experiments were performed in presence of the superoxide radical scavenger superoxide dismutase (SOD; 330 U/ml), or the hydrogen peroxide scavenger catalase (CAT; 1000 U/ml), or by adding the chain-reaction inhibitor butylhydroxytoluene (BHT; 1 mM) at selected time points. SOD, but not CAT prevented LDL peroxidation, indicating an obligatory role for superoxide radicals. Superoxide generation in this model lasts only a few minutes, however, MDA levels continued to increase over several hours. Furthermore, this phenomenon was blocked when BHT was added at various times after X/XO. These data show that LDL peroxidation is triggered by initial OR generation but then involves chain reactions which do not require continuous exposure to OR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Human low-density lipoproteins are peroxidized by free radicals via chain reactions triggered by the superoxide radical]. 166 2

1. Cultured aortic endothelial cells of the pig respond to the endothelium-derived relaxing factor (EDRF) they release with an increase in cyclic GMP content. This response is inhibited by haemoglobin or by L-NG-monomethyl-arginine (L-NMMA), and has been used to investigate the effects of phorbol esters on EDRF release. 2. Pretreatment with phorbol-12,13-dibutyrate (PDB) but not the inactive 4 alpha-phorbol-12,13,-didecanoate (PDD), inhibited increases in cyclic GMP induced by substance P (10(-8) M) in a time and concentration-dependent manner. PDB did not affect basal cyclic GMP levels. 3. PDB (3 x 10(-7) M), but not PDD (3 x 10(-7) M), also inhibited ATP (10(-5) M)-induced increases in cyclic GMP, but did not affect those induced by bradykinin (10(-7) M). 4. Increases in cyclic GMP induced by low (10(-7) M) but not high (10(-6) M) concentrations of the calcium ionophore A23187 were inhibited by PDB (3 x 10(-7) M). This inhibitory effect was due to enhanced destruction of EDRF by superoxide anions rather than inhibition of EDRF release, as the inhibition was abolished in the presence of superoxide dismutase (SOD, 30 mu ml-1) and catalase (CAT, 100 mu ml-1). 5. SOD and CAT did not affect the inhibitory action of PDB on substance P or ATP-induced increases in cyclic GMP. 6. Increases in endothelial cell cyclic GMP content induced by sodium nitroprusside (10(-5) M) were unaffected by PDB pretreatment. 7. The inhibitory effects of PDB are probably a result of an action of protein kinase C on the steps between receptor occupation and phospholipase C activation.
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PMID:Release of endothelium-derived relaxing factor from pig cultured aortic endothelial cells, as assessed by changes in endothelial cell cyclic GMP content, is inhibited by a phorbol ester. 169 49

Oxygen free radical (OFR) damage of excitable cell membranes (heart and skeletal muscle) during hemorrhagic shock and after resuscitation was studied in control rats and in rats pretreated with superoxide dismutase (SOD) and catalase (CAT; 6,000 U each) before hemorrhage. Their mean arterial pressure (MAP) was lowered to and maintained at 45 mmHg until 30% of the shed blood was spontaneously reinfused. The remaining blood and twice that volume of lactated Ringer solution were then infused. Cardiac output and organ blood flow were measured by the microsphere technique. The resting membrane potential (Em) and tissue ATP content in the heart and skeletal muscle were determined. There was no significant difference between the control and SOD + CAT groups in shock duration, maximal shed blood, hemodynamics, regional blood flow, or in ATP content in both heart and skeletal muscle, both during shock and after resuscitation. Radical scavenger treatment did not prevent muscle depolarization during shock. After resuscitation, however, significant repolarization in hearts and skeletal muscle of the SOD + CAT group (heart, -70.0 +/- 1.1; muscle, -87.0 +/- 0.6 mV) was noted when compared with the controls (heart, -62.5 +/- 1.2; muscle, -82.7 +/- 1.1 mV; P less than 0.05). This implicates OFRs as mediators of excitable cell membrane injury following resuscitation.
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PMID:Oxygen free radicals affect cardiac and skeletal cell membrane potential during hemorrhagic shock in rats. 173 25


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