Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperoxia activates superoxide dismutase (SOD) while inactivating catalase and glutathione peroxidase in polymorphonuclear leucocytes (PMN) and alveolar marcophages (AM) obtained from guinea-pigs exposed to 85% oxygen for 90 h. The influence of these altered enzyme activities on the rate of oxygen consumption and release of superoxide anion (O--2) and hydrogen peroxide (H2O2) was investigated. By 18 h O--2 released from resting PMN increased two-fold and remained elevated through the entire periods of the study, whereas H2O2 release and oxygen consumption at the same time points remained normal. At 66 h PMN phagocytizing opsonized zymosan particles released additional quantities of O--2 and H2O2 and consumed significantly more oxygen compared to the usual increase noted at earlier time points. Although oxygen consumption was almost two-fold higher in AM than PMN, phagocytizing AM released three-fold less O--2 and five-fold less H2O2 than did PMN. Furthermore, AM of animals exposed to hyperoxia no longer exhibited enhanced O--2 production upon exposure to opsonized zymosan. Hydrogen peroxide release progressively decreased at rest but progressively increased during phagocytosis of opsonized zymosan during the 90 h exposure to hyperoxia. No changes in oxygen consumption of AM occurred during hyperoxia. The divergent oxidative responses in PMN and AM of guinea-pigs exposed to hyperoxia suggest different biochemical adaptive mechanisms.
 ...
PMID:Effect of hyperoxia on superoxide anion and hydrogen peroxide production of polymorphonuclear leucocytes and alveolar macrophages. 19 22

In female Sprague Dawley rats, the tissue protein is homogeneously distributed and significantly increased in 7,12-dimethylbenz[a]anthracene-initiated mammary carcinoma. At the centre and margin of the carcinoma, the concentration of superoxide dismutase is 54 +/- 10 and 117 +/- 38 microgram/g, respectively, while in the tumour as a whole it is 104 +/- 32 microgram/g. The latter value is not significantly different from 113 +/- 35 microgram/g, the enzyme concentration in mammary tissue from lactating rats. Exposure of the tumour-bearing rats to hyperoxia does not increase the tumour protein but raises the enzyme concentration at the centre and margin of the carcinoma to 162 +/- 73 and 286 +/- 103 microgram/g, respectively.
 ...
PMID:Modification of superoxide dismutase in rat mammary carcinoma. 40 51

Adult rats show evidence of severe lung damage after 72h of continuous exposure to hyperoxia (96-98% O2). Treatment of adult rats with a solution of Plasmanate, inadvertently contaminated with endotoxin-producing organisms, or with purified endotoxin itself markedly altered the lung toxicity associated with hyperoxic exposure (survival in treated animals = 110/113 [97%] versus survival in untreated animals = 56/172 [33%]). After 72h of hyperoxic exposure, the endotoxin-treated rats demonstrated significant increases in lung superoxide dismutase, catalase, and glutathione peroxidase activity, a protectant enzyme response not seen in untreated adult rats. The basis for endotoxin's protective effect from hyperoxic lung damage is believed to be related to the stimulated increase in activity of the pulmonary antioxidant enzyme defense system. Some previously known actions of endotoxin are speculated to also serve a protective function by opposing some of the usual detrimental effects of high concentrations of O2 on the lung.
 ...
PMID:The role of endotoxin in protection of adult rats from oxygen-induced lung toxicity. 62 Dec 74

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

Mammalian cells may be protected from damage by hyperoxia through the induction of enzymes that reduce destructive oxygen-free radicals. One such enzyme is superoxide dismutase, which reduces superoxide to form hydrogen peroxide and O2. We studied the concentration of this enzyme in rat alveolar macrophages exposed to 85 to 90 per cent O2 in vitro for as long as 6 days and in macrophages obtained from rats exposed to 85 to 97 per cent O2 in vivo for as long as 7 days. In no case was there an increase in superoxide dismutase in rat alveolar macrophages, despite a doubling of superoxide dismutase in whole lungs of rats exposed to 85 to 90 per cent O2 for 7 days in vivo. We concluded that the macrophage of the adult rat does not defent itself against hyperoxia by the induction of superoxide dismutase and does not participate in the increased superoxide dismutase activity of lungs of these animals exposed to hyperoxia.
 ...
PMID:Absence of inductive effect of hyperoxia on superoxide dismutase activity in rat alveolar macrophages. 67 52

Neonatal and adult animals of five species were exposed to 95+% O2. Survival time and changes in lung antioxidant enzyme activity (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GP)) in response to hyperoxia were determined. Adult animals succumbed to O2 lung toxicity in 3--5 days. Neonatal rats, mice and rabbits showed minimal lung changes after 7 days of hyperoxic exposure and these same neonatal animals showed rapid and significant increases in lung antioxidant enzyme activities. In contrast, neonatal guinea pigs and hamsters had no lung antioxidant enzyme response to hyperoxia and these neonates died in 95+% O2 as readily as their respective parent animals. Results from an in vitro hyperoxic exposure system suggest that the lack of enzymic response of the guinea pig (and hamster) neonates to O2 challenge is due to an inherent pulmonary biochemical unresponsiveness rather than to a deficiency of a necessary "serum factor." The results of this species and age study support the important role of the lung antioxidant enzyme defense system in protection of the lung from O2-induced injury.
 ...
PMID:Oxygen toxicity in neonatal and adult animals of various species. 73 May 65

The influence of ambient O2 tensions and of cell maturation on superoxide dismutase activity were studied in tissue culture--maintained mouse alveolar macrophages. Cultivation under hyperoxic conditions (PO2 about 640 mmHg) for 24 hours was associated with a significant increase in superoxide dismutase activity as compared with normoxic conditions (PO2 approximately 150 mmHg). (Hyperoxia: superoxide dismutase = 7.9 +/- 4.0 (SD); normoxia: superoxide dismutase = 4.4 +/- 1.7 units X mg cell protein-1 P less than 0.05). Hypoxic exposure (PO2 approximately 15 mmHg) was associated with a significant decrease in superoxide dismutase compared to normoxic controls (hypoxia: 2.2 +/- 0.6; normoxic: 3.8 +/- 0.6 units X mg protein-1 P less than 0.01). This decrease was found only after 168 hours of in vitro hypoxia. The in vitro maturation of alveolar macrophages cultivated in air was associated with a progressive increase in superoxide dismutase activity per 10(6) cells, although superoxide dismutase activity per unit protein remained constant. Molecular O2 may modify cell superoxide dismutase activity by altering intrinsic enzyme regulation. The increase in superoxide dismutase activity with hyperoxia and the decrease with hypoxia are consistent with but not unequivocally establish an important role for superoxide dismutase in protecting against cellular O2 toxicity.
 ...
PMID:Effect of hyperoxia, hypoxia, and maturation on superoxide dismutase activity in isolated alveolar macrophages. 84 41

Single injection to mice of a perified preparation of superoxide dismutase (1000 units, intravenously) combined with catalase (0.5 mg) or without it failed to protect from the toxic action of 100% oxygen under the pressure of 5 ata. 1,4-diazobicyclo (2.2.2) octane (6 mg, intraperitoneally) increased the preconvulsive survival period of mice under these conditions. The formation of single oxygen under hyperoxia in vivo is supposed.
 ...
PMID:[Effect of exogenous superoxide dismutase and 1,4-diazobicyclo-(2,2,2,)-octane on the resistance of mice to acute oxygen poisoning]. 85 14

Development of toxic manifestations in rats under conditions of hyperoxia was accompanied by a significant lowering of the rat erythrocyte superoxide dismutase activity. The incubation of control rats hemolysate with hydrogen peroxide (10(-3)M) or with kumole peroxide (1.6 10(-4)M) also led to pronounced fall of the initial erythrocyte superoxide dismutase activity. As supposed, the lowering of the erythrocyte superoxide dismutase activity under hyperoxia could be due to the formation of peroxidation products.
 ...
PMID:[Study of rat erythrocyte superoxide dismutase activity during a toxic regimen of interrupted hyperbaric oxygenation]. 102 97

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


1 2 3 4 5 6 7 8 9 10 Next >>