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

Spermatogenesis is inhibited in Balb/C mice as a result of oxyradical insult. However, mammalian spermatocytes and synaptonemal complexes retain their structure and function after oxyradical insult due to protection afforded by the antioxidant vitamin E. Control groups were compared with experimental groups which were fed various vitamin E-deficient diets and subjected to varying times in an humidified 100% oxygen (hyperoxia) chamber. Measurements were made of sex body volume (SBV), nuclear envelope aberrations (NEA), and synaptonemal complex structure in spermatocytes during pachytene of meiosis prophase I. Changes in the volume of the sex body were positively correlated with increased oxyradical insult. The structure of the synaptonemal complex was not altered in any of the experimental groups which is a significant observation. It is suggested that vitamin E affords antioxidant protection and inhibits the alteration of membranes and sex chromosomes in mice during meiosis.
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PMID:Sex bodies and synaptonemal complexes of Balb/C mice: antioxidant intervention of oxyradical insult. 1121 32

Retinopathy of prematurity (ROP) is a major problem in both highly developed countries and countries with emerging technology. The incidence of ROP has been stable over the last 2 decades despite improvements in neonatology. Threshold ROP occurs in about 5% of premature infants in the US with birthweights <1.25kg. Despite treatment, a sizable minority will become blind (up to 20 to 30%). The pathophysiology of ROP can be separated into 2 phases. Phase I is hyperoxia-vasocessation. Phase II is hypoxia-vasoproliferation. The former occurs immediately following premature birth. The provision of supplemental oxygen causes retinal hyperoxia, a down regulation of vascular endothelial growth factor (VEGF) and a consequent cessation of normal retinal vascularisation. Systemic factors and increasing retinal metabolic demands cause a shift to phase II when a relative retinal hypoxia develops. This hypoxia stimulates VEGF production, leading to renewed vascularisation. This can be the resumption of normal vascularisation or abnormal neovascularisation, depending on local retinal responses. The management of ROP begins with a reliable evidence-based screening protocol. All interested parties must cooperate in developing and implementing foolproof screening protocols. Hospital officials, nursery personnel, neonatologists and ophthalmologists all have areas of responsibility in ensuring adequate screening. ROP management involves prevention, interdiction and correction. Prevention includes: adequate prenatal care which minimises premature birth, and appropriate systemic intensive care which lessens the tissue hyperoxia/hypoxia swings. Pharmacological vitamin E supplementation has largely been abandoned and ambient light reduction has been shown to be ineffective. The value of inositol supplementation and angiogenesis inhibitors in preventing ROP is presently under investigation. Interdiction concentrates on ablation of the peripheral avascular retina, thus dramatically decreasing VEGF production. Both cryotherapy and laser photocoagulation are effective; however, unfortunately, poor outcomes persist despite treatment. Supplemental oxygen administration has so far proven ineffective in limiting ROP progression. Finally, correction focuses on vitrectomy/retinal detachment repair. While anatomically successful, this procedure is often unsuccessful in terms of restoration of vision (<5% success rate). In conclusion, despite improvements in neonatology, ROP, potentially leading to blindness, continues to be a common problem associated with prematurity. Future management success must concentrate on discovering new modes of treatment, especially prevention.
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PMID:The management of retinopathy of prematurity. 1135 98

Pre-term neonates and neonates in general exhibit physiological vitamin E deficiency and are at increased risk for the development of acute lung diseases. Apoptosis is a major cause of acute lung damage in alveolar type II cells. In this paper, we evaluated the hypothesis that vitamin E deficiency predisposes alveolar type II cells to apoptosis. Therefore, we measured markers of apoptosis in alveolar type II cells isolated from control rats, vitamin E deficient rats and deficient rats that were re-fed a vitamin E-enriched diet. Bax and cytosolic cytochrome c increased, and the mitochondrial transmembrane potential and Hsp25 expression was reduced in vitamin E deficiency. Furthermore, increased DNA-fragmentation and numbers of early and late apoptotic cells were seen, but caspases 3 and 8 activities and expression of Fas, Bcl-2, Bcl-x and p53 remained unchanged. Vitamin E depletion did not change the GSH/GSSG ratio and the activities of antioxidant enzymes. Thus, vitamin E deficiency may induce a reversible pro-apoptotic response in lung cells and sensitise them for additional insult. In agreement with this hypothesis, we demonstrate that in vivo hyperoxia alone does not induce apoptosis in type II cells of control rats but reversibly increases DNA-fragmentation and numbers of early apoptotic type II cells in vitamin E-depleted cells.
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PMID:Vitamin E deficiency sensitizes alveolar type II cells for apoptosis. 1206 53

Oxidants play an important role in the development of acute and chronic lung injuries. Alveolar surfactant is the first target of air-borne oxidants. Surfactant contains, besides dipalmitoyl phosphatidylcholine, cholesterol and polyunsaturated phospholipids that play an important functional role. Therefore, vitamin E could be important for protecting surfactant lipids against oxidation and subsequent lung injury. Alveolar type II cells play a central role in synthesis and secretion of surfactant lipids and also supplement the surfactant with vitamin E during intracellular assembly. High density lipoprotein (HDL) is the primary source of vitamin E for type II cells. The uptake of vitamin E by specific lipid transfer is mediated by at least three HDL-specific receptors (scavenger receptor BI, membrane dipeptidase, and HDL-binding protein-2). In addition, cubilin and megalin mediate in a cooperative manner HDL-holoparticle uptake by alveolar type II cells. A temporary vitamin E deficiency induces a reversible change of the expression of pro- and antiinflammatory markers and of markers defining apoptosis, and reduces surfactant lipid synthesis in alveolar type II cells. These metabolic changes of type II cells may prime the lung to develop clinically manifest injury in response to an additional insult, e.g., hyperoxia.
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PMID:Vitamin E as an antioxidant of the lung: mechanisms of vitamin E delivery to alveolar type II cells. 1247 Oct 91

In order to elucidate the oxidative damage in rat brain caused by oxidative stress, regional changes in the levels of lipid peroxidation products and antioxidative defense systems in cerebral cortex and hippocampus, and in their synapses, which modulate learning and memory functions in the brain, were studied. When rats were subjected to hyperoxia as an oxidative stress, thiobarbituric acid reactive substance (TBARS) in the regions studied increased more than in normal rats by approximately 35%. The values in oxygen-unexposed vitamin E-deficient rats were also higher than in normal rats. It was found that the TBARS contents in synaptosomes isolated from both regions were remarkably higher than in the organs. These results imply that synapses are more susceptible to oxidative stress than the organ itself. This tendency was also observed in the content of conjugated diene. In response to oxidative stress, the status of the antioxidant defense system in each region, i.e. the concentration of vitamin E, and the activities of superoxide dismutase, catalase and glutathione peroxidase, decreased remarkably. On the other hand, in oxygen-unexposed vitamin E-deficient rats, the activities of these enzymes each region tended to increase, except for catalase activity. These results suggest that in response to the oxidative stress, the antioxidant defense systems may be consumed to prevent oxidative damage, and then, may be supplied through the antioxidant network.
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PMID:Oxidative damage of rat cerebral cortex and hippocampus, and changes in antioxidative defense systems caused by hyperoxia. 1274 30

Morphological alterations in the lungs of rats deficient in either or both of vitamin E and essential fatty acids were investigated after exposure to hyperoxia for 48 h. In rats deficient in both vitamin E and essential fatty acids, there was damage to type-2 alveolar cells observed as swollen mitochondria and bleb formation in the cytoplasm. None of these changes was found in rats deficient in only one of these substances. Hyperoxia in rats deficient in both substance also caused destruction of the capillary endothelial cells and edema in the interstitium. The lungs of rats deficient in only one of the substances showed some edema in the capillary endothelial cells, but not destruction, and less interstitial edema. These findings suggest that simultaneous deficiency in vitamin E and essential fatty acids facilitates lung damage in rats exposed to hyperoxia.
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PMID:The effect of hyperoxia on the lungs of rats deficient in essential fatty acids. 1523 31

The mRNA levels of three antioxidant genes, Cu/Zn superoxide dismutase (SOD), catalase (CAT) and phospholipid hydroperoxide glutathione peroxidase (GSH-Px), were quantified with real-time qRT-PCR in liver of Atlantic salmon Salmo salar exposed to 80% (normoxia), 105% and 130% O2 saturation for 54 days. The salmon were then translocated and exposed to 90% and 130% O2 saturation for additional 72 days during smoltification. TBARS and vitamin E levels in liver and the levels of oxidized glutathione (GSSG), total glutathione (GSH) and the resulting oxidative stress index (OSI) in blood were quantified as traditional oxidative stress markers. No significant mean normalized expression (MNE) differences of SOD, CAT or GSH-Px were found in liver after hyperoxia exposure at the two sampling times. Significantly decreased OSI was found in smolt exposed to 130% O2 saturation after 126 days (n = 18, P < 0.0001), indicating hyperoxia-induced oxidative stress. No effects were seen on growth, or on the levels of thiobarbituric reactive substances (TBARS) and vitamin E in liver after the exposure experiment. Overall, the mRNA expression of SOD, CAT and GSH-Px in liver related poorly with the hyperoxic exposure regimes, and more knowledge are needed before the expressed levels of these antioxidant genes can be applied as biomarkers of hyperoxia in Atlantic salmon.
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PMID:mRNA expression of antioxidant enzymes (SOD, CAT and GSH-Px) and lipid peroxidative stress in liver of Atlantic salmon (Salmo salar) exposed to hyperoxic water during smoltification. 1610 25

To elucidate whether oxidative stress induces cognitive deficit, and whether nerve cells in the hippocampus, which modulates learning and memory functions in the brain, are damaged by oxidative stress and during aging, the influence of hyperoxia as oxidative stress on either the cognitive function of rats or the oxidative damage of nerve cells was investigated. Young rats showed better learning ability than both old rats and vitamin E-deficient young rats. Vitamin E- supplemented young rats showed similar ability to young control rats. After they learned the location of the platform in the Morris water maze test, the young rats and vitamin E-supplemented young rats were subjected to oxidative stress for 48 h, and the old rats and vitamin E-deficient young rats were kept in normal atmosphere. The memory function of the old rats and vitamin E-deficient young rats declined even when they were not subjected to oxidative stress for 48 h. In contrast, the young rats maintained their memory function for 4 days after the oxidative stress. However, their learning abilities suddenly declined toward that of the normal old rats after 5 days. At this point, nerve cell loss and apoptosis were observed in the hippocampal CA 1 region of young rats. Vitamin E-supplementation in the young rats prevented either memory deficit or the induction of delayed-type apoptosis. The old rats and vitamin E-deficient young rats kept in normal atmosphere for 48 h also showed apoptosis in the hippocampus. Also, 10 days after oxidative stress, amyloid beta-like substances appeared in the CA-1 region of control young rats; these substances were also observed in the CA-1 region of the old rats and vitamin E- deficient young rats. These results suggest that reactive oxygen species (ROS) generated by oxidative stress induced amyloid beta-like substances and delayed-type apoptosis in the rat hippocampus, resulting in cognitive deficit. Since amyloid beta in Alzheimer's disease characterized by cognitive deficit induces neuronal cell death, it is reasonable to consider that amyloid beta deposition in the brain may be associated with memory dysfunction. The results of this study imply that age-related hippocampal neuronal damage is prevented by vitamin E supplementation due to the antioxidant effect of vitamin E.
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PMID:Appearance of amyloid beta-like substances and delayed-type apoptosis in rat hippocampus CA1 region through aging and oxidative stress. 1634 88

Pulmonary oxidant stress plays an important pathogenetic role in disease conditions including acute lung injury/adult respiratory distress syndrome (ALI/ARDS), hyperoxia, ischemia-reperfusion, sepsis, radiation injury, lung transplantation, COPD, and inflammation. Reactive oxygen species (ROS), released from activated macrophages and leukocytes or formed in the pulmonary epithelial and endothelial cells, damage the lungs and initiate cascades of pro-inflammatory reactions propagating pulmonary and systemic stress. Diverse molecules including small organic compounds (e.g. gluthatione, tocopherol (vitamin E), flavonoids) serve as natural antioxidants that reduce oxidized cellular components, decompose ROS and detoxify toxic oxidation products. Antioxidant enzymes can either facilitate these antioxidant reactions (e.g. peroxidases using glutathione as a reducing agent) or directly decompose ROS (e.g. superoxide dismutases [SOD] and catalase). Many antioxidant agents are being tested for treatment of pulmonary oxidant stress. The administration of small antioxidants via the oral, intratracheal and vascular routes for the treatment of short- and long-term oxidant stress showed rather modest protective effects in animal and human studies. Intratracheal and intravascular administration of antioxidant enzymes are being currently tested for the treatment of acute oxidant stress. For example, intratracheal administration of recombinant human SOD is protective in premature infants exposed to hyperoxia. However, animal and human studies show that more effective delivery of drugs to cells experiencing oxidant stress is needed to improve protection. Diverse delivery systems for antioxidants including liposomes, chemical modifications (e.g. attachment of masking pegylated [PEG]-groups) and coupling to affinity carriers (e.g. antibodies against cellular adhesion molecules) are being employed and currently tested, mostly in animal and, to a limited extent, in humans, for the treatment of oxidant stress. Further studies are needed, however, in order to develop and establish effective applications of pulmonary antioxidant interventions useful in clinical practice. Although beyond the scope of this review, antioxidant gene therapies may eventually provide a strategy for the management of subacute and chronic pulmonary oxidant stress.
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PMID:Antioxidant strategies in respiratory medicine. 1640 15

Influence of oxidative stress on fusion of pre-synaptic plasma membranes with phosphatidylcholine (PC) liposomes as a model of synaptic vesicle was investigated. The inhibitory effect of vitamin E on the decline in the fusion caused by oxidative stress was also assessed. Rats subjected to hyperoxia as oxidative stress showed significant increases in the levels of lipid hydroperoxides and protein carbonyl moieties in pre-synaptic plasma membranes in the brain. The zeta potential of pre-synaptic membrane surface was decreased markedly. When synaptosomes were incubated with PC liposomes labeled by either rhodamine B or calcein as a fluorescence probe, or 12-doxyl stearic acid as an ESR spin trapping agent, translocation of each probe into oxidatively damaged pre-synaptic membranes was decreased significantly. Fatty acid composition analysis in pre-synaptic membranes obtained from normal rats revealed a marked increase in linoleic acid and a moderate decrease in docosahexaenoic content after the incubation with liposomes. However, rats subjected to hyperoxia did not show marked changes in these fatty acid contents in their pre-synaptic membranes after the incubation. Such changes caused by hyperoxia were inhibited by vitamin E treatment of rats. These results suggest that oxidative damage of pre-synaptic membranes caused by oxidative stress lowers the lipid-mixing for the membrane fusion. The results of this study imply that vitamin E prevents the deficit in neurotransmission at nerve terminals due to the decline in fusion between pre-synaptic membrane and synaptic vesicles caused by oxidative membrane damage.
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PMID:Influence of oxidative stress on fusion of pre-synaptic plasma membranes of the rat brain with phosphatidyl choline liposomes, and protective effect of vitamin E. 1708 50


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