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

In this study, we have used the rat model of hyperoxia to examine the molecular responses to oxidative stress in lung. We show that in addition to the antioxidant enzyme manganese superoxide dismutase, expression of a variety of stress-responsive genes including heme oxygenase-1, c-fos, c-jun, CAAT-enhancer binding protein (C/EBP)-beta, and C/EBP-delta were increased after hyperoxia. Increased c-fos, c-jun, C/EBP-beta, and C/EBP-delta mRNA expression was correlated with increased DNA binding activity of the transcription factor complexes activator protein 1 and C/EBP in tissue lysates. Because oxidative damage plays an important role in the aging process and little is known about the susceptibility of aged rats to hyperoxia, we also examined the relative tolerance of old rats to hyperoxia. Surprisingly, we observed that aged rats exhibit greater tolerance to hyperoxic stress than young rats. Old rats exhibited decreased arterial oxygen tension when compared to young rats after hyperoxia exposure. This increased tolerance coincided with decreased albumin levels in bronchoalveolar lavage and the delayed onset of activation of transcription factors and expression of oxidative stress-inducible genes in old rats. Transcription factor and stress-response gene activation may serve as useful molecular markers for oxidant lung injury.
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PMID:Molecular responses to hyperoxia in vivo: relationship to increased tolerance in aged rats. 759 40

The effects of neocortical spreading depression (SD) on the expression of immunoreactive c-fos protein were examined within the superficial laminae of trigeminal nucleus caudalis (TNC), a brainstem region processing nociceptive information. KCl was microinjected into the left parietal cortex at 9 min intervals over 1 hr, and SD was detected by a shift in interstitial DC potential within adjacent frontal cortex. The stained cells in lower brainstem and upper cervical spinal cord were counted on both sides after tissues were sectioned (50 microns) and processed for c-fos protein-like immunoreactivity (LI) using a rabbit polyclonal antiserum. C-fos protein-LI was visualized in the ventrolateral TNC, chiefly in laminae I and Ilo and predominantly within spinal segment C1-2 (e.g., -1.5 to -4.5 mm from obex) ipsilaterally. SD significantly increased cell staining within ipsilateral TNC. The ratio of cells in laminae I and Ilo on the left: right sides was 1.32 +/- 0.13 after 1 M KCl, as compared to 1.06 +/- 0.05 in control animals receiving 1 M NaCl instead of KCl microinjections (p < 0.01). The ratio was reduced to an insignificant difference after chronic surgical transection of meningeal afferents and recurrent SD (1.09 +/- 0.11). Pretreatment with intravenous sumatriptan, a 5-HT1-like receptor agonist that selectively blocks meningeal C-fibers and attenuates c-fos protein-LI within TNC after noxious meningeal stimulation, also reduced the ratio to an insignificant difference (1.10 +/- 0.09). Sumatriptan or chronic surgical transection of meningeal afferents, however, did not reduce the ability of KCl microinjections to induce SD. On the other hand, combined hyperoxia and hypercapnia not only reduced the number of evoked SDs from 6.3 +/- 1.0 to 2.5 +/- 1.2 after 0.15 M KCl microinjection, but also significantly (p < 0.01) reduced associated c-fos protein-LI in TNC. These data indicate that multiple neocortical SDs activate cells within TNC. The increase in c-fos protein-LI, observed predominantly ipsilaterally, was probably mediated by SD-induced stimulation of ipsilaterally projecting unmyelinated C-fibers innervating the meninges. If true, this is the first report demonstrating that neurophysiological events within cerebral cortex can activate brainstem regions involved in the processing of nociceptive information via trigeminovascular mechanisms.
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PMID:Neocortical spreading depression provokes the expression of c-fos protein-like immunoreactivity within trigeminal nucleus caudalis via trigeminovascular mechanisms. 838 35

Apoptosis has been hypothesized to be mediated through the induction of free radicals via oxidative pathway. In this study, we demonstrated the induction of cellular apoptosis by anoxia-hyperoxia shift, but not by anoxia or hyperoxia alone in NIH3T3 cells. The decrement of ROS by anoxia thus appears to be an essential early event leading to apoptosis. G1 arrest was detected in anoxia-treated cells, and postanoxic oxygen recovery could reverse this effect, and induce apoptosis. On analysis of the binding activity of AP-1, we found biphasic induction of binding ability in cells undergoing anoxia-hyperoxia shift. In the early stage of anoxia, a transitional increase of AP-1 binding activity was detected, which was reduced to the minimal levels after 24 h of anoxia. During the period of postanoxic hyperoxia treatment, the binding activity of AP-1 was reinduced and increased remarkably with time up to 24 h. These results were in accordance with the expressions of c-jun and c-fos proteins. Enhancement of poly(ADP-ribosyl)ation activities, especially ADP-ribosylation of histone H1 was detected in post-anoxic hyperoxia-treated cells, and cleavage of PARP and activation of caspase 3 were also observed in post-anoxic hyperoxia (recovery) treated cells, but not in anoxia-treated cells. We propose that the differential induction of c-jun/c-fos (AP-1) gene expressions and sequential activation of PARP activity are essential in anoxia/hyperoxia-induced apoptosis.
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PMID:Elevation of apoptotic potential by anoxia hyperoxia shift in NIH3T3 cells. 1048 34

The aim of this work was to demonstrate the role of interferon alpha (IA) in apoptosis control of cells of hypothalamohypophysial adrenocortical system (HHAS) in young and old mice under conditions of hyperoxia. The increase of functional activity of neurosecretory cells of hypothalamic paraventricular nucleus in old mice treated with IA was demonstrated, while no effect was found in young mice. This differences could be associated with aging changes in HHAS in intact old animals. Oxidative stress caused an increase in the number of cells synthesizing proapoptotic c-fos protein in paraventricular nucleus of mice of both age groups. However, the protective action of IA against the stress is expressed more actively and in more early stage of apoptosis in young mice. Thus, the degree of IA participation in the control of programmed cell death of hypothalamic cells depends on the age of the animal. In the adrenal zona fasciculata of young mice the number of apoptotic cells was significantly increased after IA administration while after hyperoxia or its combination with IA it remained at control level. In the adrenal gland of old mice the proportion of apoptotic cells was not different from that found in young mice and remained unchanged after all experimental challenges.
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PMID:[Role of alpha-interferon in regulation of apoptosis in cells of the hypothalamo-hypophyseal-adrenocortical system of old mice in oxidative stress]. 1508 73

The aim of this study was to identify the involvement of interferon-alpha (IA) in controlling apoptosis of cells of the hypothalamo-hypophyseal-adrenocortical system (HHACS) in young and aged mice in conditions of hyperoxia. Oxidative stress led to increases in the numbers of cells synthesizing the proapoptotic protein c-fos in the paraventricular nucleus in mice of both age groups. However, the protective actions of IA in stress were more marked at the earlier stage of apoptosis in young mice. Thus, the level of involvement of IA in controlling programmed cell death of hypothalamic cells depends on the age of the animals. In the fascicular zone of the adrenals in young mice, the number of dying cells was significantly greater after administration of IA, but remained at the control level in conditions of hyperoxia alone and in combination with IA. The proportion of apoptotic cells in the adrenals of aged mice was no different from that in young mice and did not change in response to any of the treatments used.
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PMID:Involvement of interferon-alpha in the regulation of apoptosis of cells of the hypothalamo-hypophyseal-adrenocortical system of aged mice in oxidative stress. 1592 63

Treatment of hamsters with nitrosamines and hyperoxia (60% O2) induces neuroendocrine lung tumors. Analysis of 8 different tumors from 7 different hamsters demonstrated 2- to 3.5-fold increases in the expression of c-myc in 4 of 8 tumors, c-fos in 3 tumors, c-jun in 1 tumor, c-raf in 1 tumor, and Ki-ras in 2 tumors. No overexpression of the c-src and Ha-ras gene transcripts were detected. Expression levels of N-myc, p53 and the retinoblastoma gene transcript were too low to be quantitated accurately. In some cases, slightly elevated levels of protooncogene transcripts (less than 2-fold) were detected in normal-appearing tissue isolated from the same tumor bearing hamsters. Hyperoxia alone had little effect on the expression of c-myc or c-fos RNA transcripts compared to untreated hamsters. Reverse transcription of the RNAs and amplification of the cDNA copies by the polymerase chain reaction, followed by selective oligonucleotide hybridization with normal and mutant probes, did not reveal any mutations in the 12th, 13th, or 61st codons of the seven tumors which produced Ki-ras cDNA. An additional 8 tumors were also screened for Ki-ras mutations following amplification of genomic DNA and demonstrated an absence of point mutations at the Ki-ras gene locus. These results indicate that the hamster neuroendocrine lung tumors exhibit slight increases in c-myc and c-fos RNA expression but lack mutations at the Ki-ras gene locus.
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PMID:Molecular characterization of neuroendocrine lung-tumors induced in hamsters by treatment with nitrosamines and hyperoxia. 2156 81

The mechanism of oxygen toxicity for central nervous system and hyperbaric oxygen (HBO) seizure has not been clarified. Noradrenergic cells in the brain may contribute to HBO seizure. In this study, we defined the activation of noradrenergic cells during HBO exposure by c-fos immunohistochemistry. Electroencephalogram electrodes were pre-implanted in all animals under general anesthesia. In HBO seizure animals, HBO was induced with 5 atm of 100% oxygen until manifestation of general tonic convulsion. HBO non-seizure animals were exposed to 25 min of HBO. Control animals were put in the chamber for 120 min without pressurization. All animals were processed for c-fos immunohistochemical staining. All animals in the HBO seizure group showed electrical discharge on EEG. In the immunohistochemistry, c-fos was increased in the A1, A2 and A6 cells of the HBO seizure group, and in the A2 and A6 cells of the HBO non-seizure group, yet was extremely low in all three cell types in the control group. These results suggest the participation of noradrenaline in HBO seizure, which can be explained by the early excitement of A1 cells due to their higher sensitivity to high blood pressure, hyperoxia, or by the post-seizure activation of all noradrenergic cells.
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PMID:The excitement of multiple noradrenergic cell groups in the rat brain related to hyperbaric oxygen seizure. 2170 13