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

---

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

Neonatal rats (4--7 days old) and adult rats (approximately 80 days old) were continuously exposed to either 96--98% oxygen or air. Examination of the lungs of neonatal rats, who survived 5 days of oxygen exposure with no evidence of respiratory distress, showed significant increases in the pulmonary superoxide dismutase (SOD) activity (peak value: 144% of air-exposed controls), glutathione peroxidase (GP) activity (126%), glutathione reductase (GR) activity (122%), reduced glutathione (GSH) level (176%), and glucose-6-phosphate dehydrogenase activity (151%). Adult rats, most of whom succumbed within 3 days of oxygen exposure, did not show any significant increase in the activities of pulmonary SOD, GP, GR, and the level of GSH as compared to the air-exposed adult animals. Glucose-6-phosphate dehydrogenase was significantly elevated in the 72-hr oxygen-exposed adult rats. It is concluded that increases in the lung complement of SOD, GR, GP, and GSH in the neonatal rat during oxygen challenge may provide the mechanism(s) for their increased tolerance to hyperoxia-induced lung injury as compared to the adults.
...
PMID:Oxygen toxicity: comparison of lung biochemical responses in neonatal and adult rats. 64 79

Pulmonary superoxide dismutase (SOD) acitivity was determined for various groups of human fetuses, infants, and adults. Enzyme activity was found to increase with age from a low of 17 +/- 1 units/mg DNA in fetal lung to 49 +/- 6 units/mg DNA in infant lung and finally to 110.2 +/- 14.8 units/mg DNA in adult lung (P less than 0.05). No difference in lung SOD activity was demonstrated between normal infants and those with idiopathic respiratory distress/hyaline membrane disease (IRDS/HMD). No significant differences in SOD activity were found among all the samples of infant blood. Adult blood samples, however, contained significantly greater SOD activity both in terms of heme concentration and volume of whole blood (P less than 0.05). SOD activity in lung tissue from both rats and rabbits were also found to increase with age from a low value in fetal animals to a maximum activity in adults (P less than 0.05). Exposure of New Zealand White rabbits, prematurely delivered by caesarian section, to 80% oxygen for 24 hr resulted in a 42% increase in lung SOD activity. Similarly, 7-day-old Sprague-Dawley rats exposed to 85% oxygen for 24 hr showed a 43% increase in pulmonary SOD activity. No increase in pulmonary SOD was observed when adult rats were exposed to 85% oxygen for 24 hr. The effect of hyperoxia on SOD activity in excised lung was investigated. Rat lung, incubated in either heparinized whole blood or in plasma and exposed to 100% oxygen, showed a 30% increase in SOD activity after 2 hr. This capacity of lung tissue to respond to hyperoxia in vitro with increased SOD activity was age dependent. The maximum increase in SOD activity was seen with lungs from 10-12-day-old rats. The oxygen-stimulated increase in lung SOD activity disappeared at about 19-20 days of age.
...
PMID:Developmental characteristics of pulmonary superoxide dismutase: relationship to idiopathic respiratory distress syndrome. 125 Jun 44

The purpose of our present study is the possible implication of oxygen free radicals in the respiratory distress induced in rats by intravenous administration of arachidonic acid (20 mg/kg). The respiratory frequency was measured and plasma TXB2 concentration was assayed by RIA from blood withdrawn 1 min after arachidonic acid administration. The substances studied were: SOD, catalase, mannitol, DMSO, BHT, imidazole. All the drugs, except imidazole, significantly protect the rats from the respiratory distress induced by arachidonic acid. SOD, catalase, BHT and imidazole inhibit whereas mannitol and DMSO increase the plasma levels of TXB2. We suggest that oxygen free radicals generated in the respiratory burst induced by arachidonic acid are mainly responsible for the consequent respiratory distress.
...
PMID:Role of oxygen free radicals in respiratory distress induced by arachidonic acid in the rat. 190 69

To investigate O2- generation in in situ lungs of rats treated with drugs to induce experimental acute respiratory distress syndrome, phorbol myristate acetate (PMA) or endotoxin were injected into rats, who had been continuously infused with 2(methyl-6-[p-methoxyphenyl]-3,7-dihydroimidazo[1,2-alpha]pyraz in-3-one (MCLA) and the chemiluminescence in in situ lung was detected by a sensitive photon counter. In PMA-treated rats, two phases of chemiluminescence over non-specific chemiluminescence were observed. The first phase luminescence was sensitive to Cu-Zn superoxide dismutase, while the second phase chemiluminescence was less sensitive to Cu-Zn superoxide dismutase. Similar chemiluminescence was detected in the rats treated with endotoxin instead of PMA, but not in neutropenic rats.
...
PMID:The first observation of O2- generation in in situ lungs of rats treated with drugs to induce experimental acute respiratory distress syndrome. 215 28

The clinical trials performed with bovine superoxide dismutase (SOD) are reviewed. SOD, applied intraarticularly at a dosage of 2-16 mg, proved to be effective in osteoarthritis of the knee joint in three placebo-controlled and one steroid-controlled double-blind trials. Its efficacy in other inflammatory joint disorders is documented by uncontrolled trials. Similarly, some controlled and many open studies support the efficacy of locally injected SOD in periarticular inflammation. Systemic treatment of rheumatoid arthritis by SOD at the dosages indicated yielded disappointing results. Well documented, though open uncontrolled studies demonstrated beneficial effects of locally administered SOD in radiation cystitis, interstitial cystitis and Peyronie's disease. Tolerance is good, but allergic reactions at low incidence have to be anticipated. Human SOD derived from recombinant microorganisms is being developed to explore its therapeutic potential particularly in ischemia-reperfusion damage, adult respiratory distress or similar conditions.
...
PMID:Superoxide dismutase for therapeutic use: clinical experience, dead ends and hopes. 306 19

The use of high oxygen concentrations and high mean airway pressures during mechanical ventilation of premature newborn infants with respiratory distress syndrome leads in 20%-30% of the survivors to chronic lung disease. This study explores if exogenous polyethylene glycol conjugated superoxide dismutase (PEG-SOD) and catalase (PEG-CAT) mitigate oxygen toxicity in premature lambs with respiratory distress syndrome. Six pairs of premature lambs were delivered by cesarean section and treated by tracheal instillation of 60 mg natural sheep surfactant/kg/body weight. After birth, all lambs were ventilated with 100% oxygen, and one of each pair received a single intravenous injection of 1 million U/kg PEG-CAT and 50,000 U/kg PEG-SOD. At 8 h of age or after respiratory failure was established, the lambs were killed and the lungs were removed intact. Lung damage was assessed by microscopy. The arterial blood gases, pH, and mean airway pressures of the lambs treated with PEG-SOD/PEG-CAT did not differ from those of the controls. Mean PaO2 was greater than 140 mmHg during the first 4 h of the experiments. In the lambs treated with PEG-SOD/PEG-CAT, SOD and CAT levels were very high during the study period and less bronchiolar epithelial damage and lung hemorrhages were found at microscopy.
...
PMID:Prevention of oxygen toxicity with superoxide dismutase and catalase in premature lambs. 310 53

Deficiencies of antioxidant defenses have been postulated as possible mechanisms in the development of bronchopulmonary dysplasia (BPD). Neonates, especially prematures with respiratory distress syndrome (RDS), are exposed to high oxygen tensions for prolonged periods. To evaluate the neonates' ability to respond to an oxygen challenge with increased superoxide dismutase (SOD), 9 prematures were studied immediately at birth and on days 1, 3, 5, and 7. An increase in plasma levels was noted during the first week of life in the patients who were exposed to oxygen. The mean endogenous SOD level at birth was 1.28 microgram/ml. On day 1, plasma SOD rose to 1.53 microgram/ml and to 2.25 micrograms/ml on day 3 (P = .003). This trend continued into the fifth and seventh days. Whether this increase in SOD has clinical significance in the prevention of BPD requires further investigation.
...
PMID:Endogenous antioxidant defenses in neonates. 329 92

High concentrations of oxygen are administered with increased airway pressure to most preterm neonates with respiratory distress syndrome (RDS). Among 20% to 30% of survivors a form of chronic lung disease, bronchopulmonary dysplasia (BPD), develops. Its pathogenesis may include tissue damage caused by the superoxide anion (O2-) and other free oxygen radicals. Animal experiments and other data suggested a rationale for superoxide dismutase (SOD) administration in an effort to prevent or ameliorate BPD. Our preliminary studies in 19 prematures with RDS demonstrated its safety in human newborns and permitted measurement of its plasma levels. No adverse clinical findings occurred, and laboratory parameters were unchanged. Subcutaneous administration (0.25 mg/kg) of bovine SOD led to detectable levels at 1 1/2 h (mean 0.22 microgram/ml), with a slight rise to a higher peak at 2 1/2-4 h and a plateau over the remainder of the 12-h interval. Following doses 2-5, peak levels of 0.64 microgram/ml occurred at 4-8 h. With this background, a prospective double-blind controlled study of 45 neonates (mean gestational age, 29 weeks; birth weight, 1,100 g) showed a statistically significant reduction in prevalence of clinical and X-ray signs of BPD with fewer days of continuous positive airway pressure required. The safety and pharmacokinetics of bovine SOD were confirmed.
...
PMID:Oxidant-mediated lung disease in newborn infants. 329 87

The effectiveness of bovine superoxide dismutase (SOD) in the prevention of bronchopulmonary dysplasia was evaluated in a prospective double-blind controlled study in 45 neonates (mean gestational age 28.7 weeks, mean weight 1154 gm) with severe respiratory distress syndrome. All were ventilator dependent with FiO2 greater than or equal to 0.7 at 24 hours of age. Either bovine SOD (0.25 mg/kg) or saline solution was administered subcutaneously every 12 hours according to random selection until patients could be maintained in room air without ventilatory or continuous positive airway pressure (CPAP) support. SOD levels were detected in all patients given treatment. Mean peak values at 4 hours after dose ranged from 0.15 micrograms/ml (dose 1) to 0.45 micrograms/ml (dose 10). The drug was well tolerated, and no side effects were detected. Among the 31 survivors (SOD 14, placebo 17) radiologic evidence of BPD was significantly less in patients given SOD (3/14 vs 12/17, P = 0.008). Clinical signs of bronchopulmonary dysplasia (wheezing, pneumonia) were less in patients given SOD (3/14 vs 11/17, P = 0.019). Patients given SOD required fewer days of CPAP (P less than 0.003). There were no differences in days of O2 therapy, intermittent positive pressure breathing, or incidence and severity of patent ductus arteriosus or intraventricular hemorrhage. This preliminary study suggests that SOD may be helpful in reducing the severity of bronchopulmonary dysplasia in infants with respiratory distress syndrome.
...
PMID:Prevention of bronchopulmonary dysplasia by administration of bovine superoxide dismutase in preterm infants with respiratory distress syndrome. 650 11

Rats have been exposed for periods of 120 to 240 minutes to an atmosphere containing 6 +/- 0.7 mg per cu.m mercury vapor. All rats developed an acute respiratory distress which lead to death within 2 to 210 hours (mean 53.5 h). Microscopical examination of the lungs showed an oedema rich in fibrin, an epithelial necrosis, hyaline membranes and in two cases an interstitial fibrosis. Mercury levels in the lungs ranged between 0.5 and 9.37 micrograms per gramme wet weight. The activity of pulmonary superoxide dismutase was decreased to 1.57 +/- 0.66 micrograms per mg of soluble proteins, compared with the level of 5.01 +/- 0.76 micrograms per mg in control rats. This study confirm the pulmonary toxicity of mercury vapors observed in human intoxication.
...
PMID:[The pulmonary toxicity of mercury vapors in the rat]. 667 10


1 2 3 4 5 6 7 Next >>

---