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

We used a nutritional deprivation model to produce intrauterine growth-retarded (IGR) rat pups (birth weight = approximately 75% of normal). The IGR newborns evidenced a marked reduction in tolerance to greater than 95% O2 exposure: 10-day survival = 10/47 (21%) versus 18/36 (50%) for control pups, and LT50 = 7.2 days versus 10 days for controls (p less than 0.01). Various lung parameters at birth and during O2 exposure were examined to try to define why prenatal undernutrition should compromise the survival of IGR rats in hyperoxia. We found decreased lung glutathione peroxidase and glucose-6-phosphate dehydrogenase activity (with normal superoxide dismutase and catalase levels) in the IGRs at birth; decreased lung disaturated phosphatidylcholine content (even more markedly decreased in 1-day premature pups); and decreased lung surface area/body weight. These factors and other features of newborn IGRs reported in the literature may help to explain how prenatal undernutrition compromises postnatal tolerance to prolonged high-O2 exposure.
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PMID:Intrauterine growth-retarded rat pups show increased susceptibility to pulmonary O2 toxicity. 398 89

Total glutathione levels and the activity of enzymes associated with antioxidant protection in neonatal lung are increased in response to hyperoxia. Glutathione levels in developing rat lung decreased from 24 nmol/mg protein on day 19 of gestation to approximately 12 nmol/mg protein at birth. The initial decrease in glutathione may be due to emergence of other antioxidant systems. Newborn rats placed in 100% oxygen showed a rapid and sustained increase in total glutathione levels which was primarily due to an increase in reduced glutathione. Explants obtained from 16-wk gestation human fetal lung or from 17- to 18-day fetal rat lung also showed increased total and reduced glutathione when cultured in 95% oxygen, 5% CO2 as compared with explants cultured in room air. Type II cells isolated from neonatal rats maintained in oxygen for 6 days also showed glutathione levels twice those found in cells isolated from animals in room air. The activity of antioxidant enzymes (glucose-6-phosphate dehydrogenase, glutathione peroxidase, glutathione reductase) was increased in lungs of newborn rats exposed to 100% oxygen either at birth or 2 days of age. Antioxidant enzyme activity of lung explants cultured in 95% oxygen, 5% CO2 was also higher than in explants maintained in room air. These results suggest that the increases in glutathione and of antioxidant enzymes in vivo and in vitro are a direct effect of oxygen exposure in lung and that the increase of both glutathione and antioxidant enzyme activity is intrinsic to the lung cell itself. It is likely that increases in glutathione in lung represent an important protective mechanism against oxidant injury.
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PMID:The responses of glutathione and antioxidant enzymes to hyperoxia in developing lung. 403 84

Induction of two forms of superoxide dismutase, catalase and glutathione peroxidase, occurs very rapidly in neonatal rat lung tissue upon exposure of these animals to 94 + % normobaric oxygen. No such oxygen-mediated enzyme induction occurs in the lungs of adult rats. The aged-dependent pattern of enzyme induction correlates with the well-established age-dependent tolerance of neonatal rats to hyperoxia. Enzyme induction occurs in the lungs of neonates in only those species known to be resistant to oxygen-provoked lung damage. Compromise of oxygen-mediated enzyme induction predisposed the neonatal rats to pulmonary oxygen toxicity. These data have formed the basis of the proposal that oxygen induction of the superoxide dismutases catalase and glutathione peroxidase provides a vital part of the defense mechanism against oxygen toxicity. A biochemical mechanism of oxygen-provoked pulmonary damage has been elaborated to explain the role of each enzyme in the protection against oxygen and free radical toxicity.
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PMID:Proposed mechanism for neonatal rat tolerance to normobaric hyperoxia. 625 31

We tested the hypothesis that pulmonary indoleamine 2,3-dioxygenase (indole:oxygen 2,3-oxidoreductase (decyclizing), EC 1.13.11.17), an enzyme that consumes superoxide anion (O-2), might have an antioxidant role under conditions of hyperoxia. We measured indoleamine 2,3-dioxygenase in three experimental models in which pulmonary superoxide dismutase, catalase and glutathione peroxidase (the known antioxidant enzymes) show increased activity and are associated with greater tolerance to 96-98% O2 exposure: (1) adult rats preexposed to 85% O2 for 5-7 days; (2) neonatal rats exposed directly to greater than 95% O2; and (3) adult rats treated with bacterial endotoxin during O2 exposure. Indoleamine 2,3-dioxygenase did not increase in response to O2 exposure in any of these rat models. Conversely, in adult mice treated with endotoxin, lung indoleamine 2,3-dioxygenase activity did increase, but no protection against O2 toxicity occurred. Thus, a rise in indoleamine 2,3-dioxygenase is neither necessary nor sufficient to confer resistance to O2 toxicity. These data taken together are evidence against its having any important role in the antioxidant defense system of the lung.
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PMID:The activity of pulmonary indoleamine 2,3-dioxygenase in rats and mice is not altered by oxygen exposure. 628 1

Mice and rats were adjusted to daily treadmill training programs, which were heavy enough to increase the oxidative capacity of skeletal muscles. Endurance training did not affect the activities of catalase and glutathione peroxidase and the concentration of vitamin E in the lungs of mice and rats. Thus increased ventilation and oxygen utilization induced by exercise training do not modify lung antioxidants, in contrast to hyperoxia and hypoxia.
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PMID:Endurance training and antioxidants of lung. 646 85

Rats pretreated with 500 micrograms X kg-1 endotoxin are resistant to the pulmonary toxic effects of normobaric hyperoxia (greater than 95% O2). After endotoxin-pretreatment and exposure to 1.0 ATA O2 for 72 h, such rats are found to have elevated total superoxide dismutase, glutathione peroxidase, and catalase activities in homogenates of whole lungs. Despite increases in these protective antioxidant enzymes which persist in 2.0 ATA O2 (4 h) and 4.0 ATA O2 (1.0 h), such rats do not have improved survival in hyperbaric hyperoxia. Likewise, endotoxin-pretreatment immediately prior to 2.0 or 4.0 ATA O2 exposure does not prolong survival compared to controls. It is likely that lung injury during the normobaric oxygen preexposure and the central nervous system toxicity of hyperbaric oxygen interact to limit survival.
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PMID:The endotoxin-pretreated, oxygen-adapted rat model in hyperbaric hyperoxia. 648 6

The anticancer drug 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) inhibits glutathione reductase, an enzyme involved in oxidant defense systems. The 30-day LD50 for BCNU in male and female BALB/c mice was 52 and 46 mg/kg, respectively. A 35-mg/kg BCNU dose was not lethal to any animal. Glutathione reductase was inhibited in lung tissue by about 50% for 4 days following a single 35 mg/kg dose of BCNU. The prolonged inhibition of glutathione reductase by BCNU suggested this drug might enhance pulmonary oxygen toxicity by diminishing the lung's antioxidant capacity. Exposing mice treated with 35 or 50 mg/kg BCNU to continuous 85% oxygen decreased the LT50 from 13.1 to 6.3 and 5.3 days, respectively, compared to vehicle-treated controls. All mice treated with 35 mg/kg BCNU or vehicle and exposed to 85% oxygen only on Days 0-4 survived to Day 30. Extending the hyperoxic exposure 1 additional day resulted in the death of all BCNU-treated mice, while 70% of the vehicle-treated mice survived to Day 30. Pulmonary glutathione peroxidase, catalase, and superoxide dismutase activities were unaffected up to 6 days following 35 mg/kg BCNU, 85% oxygen, or both. Pulmonary glutathione reductase activity was unaffected by 85% oxygen alone, although hyperoxia extended the BCNU-induced inhibition of this enzyme to Day 6. BCNU, 35 mg/kg, had little effect on lung reduced glutathione (GSH) levels. A significant decrease was only measured on Day 4. Hyperoxia, either alone or with BCNU, had no effect on lung GSH content.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhanced oxygen toxicity following treatment with 1,3-bis(2-chloroethyl)-1-nitrosourea. 651 Jun 7

Rats treated with low doses of bacterial endotoxin have been shown to be protected from oxygen poisoning under normobaric conditions. Induction of lung activity of the antioxidant enzymes glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) has been reported to occur with endotoxin administration. GSH-Px is a selenoenzyme and selenium-deficient rats have decreased lung GSH-Px activity and enhanced lung toxicity during a hyperoxic exposure. To determine whether bacterial endotoxin administration can provide protection for animals with decreased antioxidant defenses, selenium-deficient and control rats received daily intraperitoneal injections of 250 micrograms/kg bacterial endotoxin or phosphate-buffered saline (PBS) during normobaric exposure to greater than 95% O2. Both groups of animals were protected from hyperoxia by bacterial endotoxin administration despite the extremely low lung GSH-Px activity in the selenium-deficient rats. GSH-Px, SOD, or CAT activities were not induced in the selenium-deficient rats by 48 hr (the time when the selenium-deficient rats treated with PBS began to die). In the selenium-deficient rat, mechanisms other than enzyme induction appear to be providing early protection from hyperoxia.
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PMID:Endotoxin protects selenium-deficient rats from hyperoxia. 669 Jun 38

Preexposure of adult rats to ozone (0.8 +/- 0.1 ppm for 7 days) has been found to produce a marked degree of tolerance to hyperoxia (greater than 95% O2). The survival of O3-preexposed rats in hyperoxia for 168 h was 28 of 32 (88%) compared with a rate of 2 of 18 (11%) for nonpreexposed rats. Total lung superoxide dismutase (SOD), glutathione peroxidase (GP), glucose 6-phosphate dehydrogenase (G6-PD), and catalase (CAT) activities were all significantly increased after O3 preexposure and after the subsequent hyperoxic challenge. Probable mechanisms accounting for the markedly improved survival in hyperoxia after O3 preexposure include both increased lung antioxidant enzyme and repair of structural damage by proliferation of alveolar lining cells. The demonstration of cross-tolerance between the atmospheric oxidants O3 and O2 suggests that there are similarities in the lung's adaptation to both oxidants.
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PMID:Ozone-induced tolerance to hyperoxia in rats. 670

Rats fed 3% casein diets for 6 days showed an increased susceptibility to greater than 98% oxygen [mean survival time 46.9 +/- 4.1 (SD) h] compared with animals fed 25% casein diets (mean survival time 60 +/- 5 h). The 3% casein diet did not reduce the responses to hyperoxia of lung glucose-6-phosphate dehydrogenase, glutathione peroxidase, and glutathione reductase (NAD(P)H), which maintain tissue levels of reduced glutathione or lung superoxide dismutase levels. While supplementation of the 3% casein diet with the sulfur-containing amino acids (cysteine, cystine, or methionine) prevented the increased oxygen toxicity, supplementation with leucine, a nonsulfur-containing amino acid, had no effect on potentiation of toxicity. Animals fed the unsupplemented 3% casein diet failed to show an elevation of lung glutathione in response to hyperoxia. When the 3% casein diet was supplemented with cysteine, total lung glutathione levels increased normally during oxygen exposure. Supplementation of the 25% protein diet with cysteine did not further protect these animals. We conclude that potentiation of oxygen toxicity by dietary protein deficiency in the rat is due to the low sulfur-containing amino acid content of the diet; the mechanism of increased toxicity by hyperoxia is probably related to an inability to increase glutathione levels due to a shortage of the cysteine component of the glutathione tripeptide.
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PMID:Potentiation of oxygen toxicity in rats by dietary protein or amino acid deficiency. 682 98


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