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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Superoxide dismutase is considered important in protection of aerobes against oxidant damage, and increased tolerance to oxidant stress is associated with induction of this enzyme. However, the importance of superoxide dismutase in this tolerance is not clear because conditions which promote the synthesis of superoxide dismutase likewise affect other antioxidant enzymes and substances. To clarify the role of superoxide dismutase per se in organismal defense against oxidant-generating drugs, we employed Escherichia coli transformed with multiple copies of the gene for bacterial iron superoxide dismutase. These bacteria have greater than ten times the superoxide dismutase activity of wild-type E. coli but, importantly, are normal in other oxidant defense parameters including catalase, peroxidases, glutathione, and glutathione reductase. High superoxide dismutase and control bacteria were exposed to the O2- -generating drug paraquat and to elevated pO2. We find; high superoxide dismutase E. coli are more readily killed by paraquat under aerobic, but not anaerobic, conditions. During exposure to paraquat, high superoxide dismutase E. coli accumulate more H2O2. Coincidentally, the reduced glutathione content of high superoxide dismutase E. coli declines more than in control E. coli. E. coli with high superoxide dismutase activity are also more readily killed by hyperoxia. Interestingly, the susceptibility of the parental and high superoxide dismutase E. coli to killing by exogenous H2O2 is not significantly different. Thus, under these experimental conditions, greatly enhanced superoxide dismutase activity accelerates H2O2 formation. The increased H2O2 probably accounts for the exaggerated sensitivity of high superoxide dismutase bacteria to oxidant-generating drugs. These results support the concept that the product of superoxide dismutase, H2O2, is at least as hazardous as the substrate, O2-. We conclude that effective organismal defense against reactive oxygen species may require balanced increments in antioxidant enzymes and cannot necessarily be improved by increases in the activity of single enzymes.
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PMID:Superoxide dismutase-rich bacteria. Paradoxical increase in oxidant toxicity. 354 14

Whereas guinea pigs have advanced prenatal morphological lung development, their surfactant development is not "precocious" compared with other small laboratory animals. To investigate whether maturation of the antioxidant enzyme (AOE) system coincides more closely with surfactant development or with morphological maturation, we assayed fetal guinea pig lungs at gestational days 49-69 for superoxide dismutase, catalase, and glutathione peroxidase activities. We found that elevations in pulmonary AOE occurred in parallel with increases in surfactant during the final 10-15% of gestation. Since newborn guinea pigs behave more like adult animals in their relative intolerance to hyperoxia, we explored whether prematurely delivered guinea pigs would tolerate high O2 exposure better than full-term newborns. We found that prematures have markedly improved hyperoxic tolerance compared with newborns (time at which 50% of animals died in greater than 95% O2, 6.4 days vs. 4.5 days, respectively, P less than 0.05); and (unlike newborns) premature pups are capable of mounting an elevated AOE response to hyperoxic challenge. Thus premature guinea pigs behave more like full-term newborns of other species in respect to hyperoxic tolerance, an additional precocious feature of guinea pig development.
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PMID:Guinea pig lung development: antioxidant enzymes and premature survival in high O2. 356 1

Adult rats were exposed to room air, 50%, 65%, or 80% oxygen for 6 wk. Subsets were sacrificed periodically in order to establish alterations in growth parameters and lung antioxidant responses. Prolonged exposure to 50% or 65% oxygen did not result in weight loss or changes in lung-to-body weight ratios relative to control values. Treatment with 50% oxygen produced delayed increases in nonprotein sulfhydryl (NPSH) content and catalase (CAT) activity, while treatment with 65% oxygen produced delayed increases in NPSH, CAT, and glutathione peroxidase (GPx) content. Rats treated for 6 wk with either 50% or 65% oxygen died significantly earlier than room-air control animals when these groups were subsequently exposed to 100% oxygen. Rats exposed to 80% oxygen had significantly decreased body weight, increased lung-to-body weight ratios, and increased levels of NPSH, CAT, GPx, total superoxide dismutase, and glutathione reductase by 11 days of treatment. At 6 wk they had significantly altered growth parameters and increased GPx catalase, and NPSH levels. Their final antioxidant profile was not significantly different from 65% oxygen-exposed rats. However, these animals survived significantly longer than any group when exposed to 100% oxygen. In summary, lower concentrations of sublethal hyperoxia (less than or equal to 65%) were capable of eliciting significant antioxidant enzyme responses. Levels of antioxidant enzymes in the lungs of rats chronically exposed to sublethal hyperoxia did not appear to be solely responsible for enhanced survival in subsequent lethal hyperoxia.
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PMID:Adaptation to chronic hyperoxia. Biochemical effects and the response to subsequent lethal hyperoxia. 357

An animal model was established to study the toxic effects of hyperoxia and the consequent changes in intracellular antioxidant status. Superoxide dismutase, catalase and glutathione peroxidase activities were measured in erythrocytes, liver and lung, in addition to cellular glutathione concentrations and its associated metabolism. Overt cellular damage was assessed biochemically by measurement of lipid peroxidation, hydrogen peroxide-induced haemolysis and osmotic fragility. Pathological changes were assessed by light and electron microscopy. Up to 11 days exposure of rats to 80% oxygen was not lethal, but resulted in overt cellular damage to red blood cells (haemoglobin concentration decreased from 13.8 +/- 1.4 (SD) g dl-1 to 12.4 +/- 0.5 g dl-1; hydrogen peroxide-induced haemolysis increased from 7.7 +/- 1.6% to 75.1 +/- 13.5% after 11 days of hyperoxia) and to cells of lung (4-fold increase in lipid peroxidation) as well as a biochemical adaptation to the increased concentration of oxygen metabolites (superoxide dismutase increased 3-fold, catalase 5-fold and glutathione peroxidase 2-fold). It is suggested that red cell hydrogen peroxide-induced haemolysis and reduced glutathione concentration may be useful indicators of oxidant stress in the clinical situation.
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PMID:Tissue responses to hyperoxia. Biochemistry and pathology. 360 20

We have studied the influence of hyperoxia and ageing on the activities of NADPH-cytochrome c reductase and glutathione S-transferase in different rat organs. Lung glutathione S-transferase activity increases markedly in 5-day-old pups exposed to hyperoxia, as observed for the O2- scavenging enzyme, superoxide dismutase. The levels of NADPH-cytochrome c reductase increase as well but after a 3-day lag period. In the liver, there is a pronounced decrease of both activities in 24-month-old rats, but at 12 months the activity of glutathione S-transferase increases whereas that of NADPH cytochrome c reductase activity decreases with respect to 3 months. The pattern of variations with age of NADPH cytochrome c reductase is similar in liver and brain. However the behaviour of brain glutathione S-transferase parallels that of the liver enzyme only up to 12 months. Thereafter the brain activity is maintained at a high level. These observations open the possibility that the high glutathione S-transferase levels in the old rat brain might be involved in protection towards oxidative alterations during ageing.
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PMID:Variations due to hyperoxia and ageing in the activities of glutathione S-transferase and NADPH-cytochrome c reductase. 361 86

Using a rat model, we assessed the efficacy of varying doses of superoxide dismutase of (SOD) to affect plasma and tissue SOD concentrations and to attenuate dysplastic changes of lung and pulmonary vascular growth, which are chronic sequelae of neonatal oxygen exposure. One hundred forty-three 1-day-old Sprague-Dawley rats were divided into two groups and exposed to hyperoxia (0.96 to 1.0 Fio2) or room air for 8 postnatal days. Each group was subdivided into five treatment groups, which received 6, 20, 100, or 200 mg/kg/d SOD or a placebo, intramuscularly every 12 hours. All rats were then placed in room air; 52 were killed, and lung tissue and blood samples were obtained for measurement of bovine SOD concentration. The remaining rats received routine care until 58 to 60 days of age, when functional and morphologic cardiopulmonary changes were assessed. Bovine SOD concentration of pooled plasma samples increased 26-fold, from 2 to 50 micrograms/mL, between the 6 and 200 mg/kg/d SOD groups, but mean tissue concentration increased only six-fold, from 0.34 to 2.1 micrograms/lung. Cardiovascular and pulmonary changes found in each oxygen group, regardless of SOD dosage, included elevated right ventricular pressure, increased right ventricular weight, decreased number of small pulmonary arteries/mm2, decreased number of alveoli/mm2, and increased volume proportion of lung parenchyma. Thus, high plasma concentrations of bovine SOD failed to prevent the chronic cardiovascular and pulmonary sequelae of neonatal oxygen exposure in the rat, possibly because SOD did not reach the intracellular sites of action.
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PMID:Administration of bovine superoxide dismutase fails to prevent chronic pulmonary sequelae of neonatal oxygen exposure in the rat. 364 25

Studies about the proposed antioxidant physiological role of the catalase (CAT) enzyme in relation to different environmental oxygen tensions are reported for the first time in amphibian larvae of Discoglossus pictus and Rana ridibunda perezi during their development. The CAT levels of whole tadpoles increased constantly in both species during the larval period, reaching a maximum during the metamorphic climax. All through development, CAT activity levels were always greater in D. pictus than in R. ridibunda perezi. This correlates well with the already reported higher SOD activity and hyperoxia resistance of the D. pictus species when compared to R. ridibunda perezi. Long-term acclimation to different levels of hyperoxia (40, 60, and 100% O2) showed dose-related increases in the CAT activity of D. pictus tadpoles. These increases did not take place when the animals were subjected to acute hyperoxia (24 h). The increase in CAT activity observed after 15 days of acclimation to acute hyperoxia (710 mm Hg: 100% O2) was reversed after 15 additional days of postacclimation to normal air (149 mm Hg O2). When recently metamorphosed frogs were acclimated to acute hyperoxia, significant increases in CAT activity were observed after 15 days, but not after 7 days. The results are interpreted as supporting a protective role for the CAT enzyme in amphibian larvae and froglets against oxygen toxicity.
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PMID:Different levels of hyperoxia reversibly induce catalase activity in amphibian tadpoles. 366 17

Oxygen toxicity in the non-ischemic and non-hypoxic heart has not been reported. In an experiment on isolated rat heart lung preparation, the effects of superoxide dismutase (SOD) on oxygen toxicity during hyperoxic perfusion were evaluated with intramyocardial high energy phosphates and the release of creatine phosphokinase (CPK) in the perfusate blood. Although there were no significant differences in high energy phosphates between SOD-treated and untreated hearts, the CPK release from the SOD-treated hearts was significantly less than from the untreated hearts. SOD increased the oxygen pressure of perfusate blood, too. These results indicate that hyperoxia induced cardiac and lung cell damage which was protected by SOD.
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PMID:Protective effects of superoxide dismutase against oxygen toxicity in rat's heart lung preparation. 369 65

The administration of very low doses of bacterial endotoxin protects rats during exposure to hyperoxia and is associated with the induction of lung antioxidant enzyme activities. Copper-deficient rats have increased susceptibility to O2 toxicity, which may be related to their decreased lung superoxide dismutase activity (SOD) or decreased plasma ceruloplasmin concentrations. To determine whether endotoxin can protect against hyperoxia in this susceptible model, we exposed copper-deficient and control rats to a fractional inspiratory concentration of O2 greater than 0.95 for 96 h after pretreatment with 500 micrograms/kg of bacterial endotoxin or phosphate-buffered saline (PBS). Mortality in the copper-deficient and control rats given PBS and exposed to O2 for 96 h was 100%. Copper-deficient rats died significantly earlier during the exposure than controls. No mortality occurred in either group treated with endotoxin and hyperoxia despite the decreased activity of copper-dependent enzymes in the copper-deficient rats. Copper-deficient rats treated with endotoxin and exposed to hyperoxia did increase lung Cu-Zn-SOD activity, but activity remained below levels found in air-exposed controls. Mn-SOD activity was found to be induced above air-exposed controls in the copper-deficient rats treated with endotoxin and exposed to hyperoxia. Hyperoxic exposure resulted in a marked increase in plasma ceruloplasmin concentrations in the control rats, but no increases in ceruloplasmin occurred in the copper-deficient animals. Endotoxin protects copper-deficient rats from hyperoxia despite their decreased lung Cu-Zn-SOD activity, and decreased plasma ceruloplasmin.
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PMID:Effects of bacterial endotoxin on protecting copper-deficient rats from hyperoxia. 375 84

We compared the effects of 95% O2 (hyperoxia) alone, endotoxin (20 ng/ml) alone, and 95% O2 plus endotoxin on the release of lactate dehydrogenase (LDH), uptake of 5-hydroxytryptamine (5-HT), and antioxidant enzyme activities in porcine pulmonary arterial and aortic endothelial cells in monolayer culture. Hyperoxia increased LDH release and decreased 5-HT in both endothelial cell types. Hyperoxia also caused a decrease in catalase (CAT) activity and an increase in total superoxide dismutase (SOD) and glutathione reductase (GSH-Red) activities in both cell types. Endotoxin alone had no effect on LDH release, 5-HT uptake, or antioxidant enzyme activities. However, endotoxin prevented the hyperoxic increase in LDH release and the hyperoxic decrease in 5-HT uptake. Endotoxin plus 95% O2 had no consistent effect on the antioxidant enzyme profile in pulmonary artery or aortic endothelial cells. These results indicate that (1) hyperoxia injures both pulmonary artery and aortic endothelial cells in culture and causes changes in the antioxidant enzyme profile that are similar in the two cell types; (2) hyperoxia-induced decreases in CAT activity and increases in SOD activity may be responsible for increased sensitivity of endothelial cells to O2 toxicity; and (3) endotoxin protects against hyperoxic injury to endothelial cells in vitro, but increases in antioxidant enzyme activities are not the mechanism for this protection.
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PMID:Effect of oxygen and endotoxin on lactate dehydrogenase release, 5-hydroxytryptamine uptake, and antioxidant enzyme activities in endothelial cells. 388 60


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