Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is apparent from the above discussion that acute stress, such as ischemia and reperfusion, hypoxia and reoxygenation, hyperthermia and oxidative stress, can rapidly potentiate the induction of genes for certain members of the HSP families and for antioxidants/antioxidant enzymes. Whether the stress response and induction of these genes have a direct role in myocardial protection is not known, but the induction of the expression of these genes are mostly associated with the preservation of myocardial cells from subsequent injury resulting from ischemia, hypoxia and reperfusion. The ubiquitous presence of some of these stress genes, such as for HSP 70 and catalase, in normal unstressed myocardium further suggests a role of these genes in many basic and essential biochemical and metabolic pathways. It is reasonable to speculate that the cells respond to the stress as a consequence of perturbations of one or more of the metabolic pathways by stimulating the induction of the stress genes of that particular pathway in which they participate. Thus, these genes are likely to be involved both in the protection and recovery/repair mechanisms. The precise mechanism by which myocardial cell recognizes and responds to a particular stress agent such as ischemia, hypoxia, hyperthermia or oxidative stress is not clear. While it is tempting to speculate that a generalized mechanism exists, applying to all different modes of stress response and gene induction, whether these agents induce the response via independent pathways or converge within a single point is entirely unclear. However, from the striking resemblance between the pattern of gene expression, especially with regard to HSP and antioxidant genes, it is reasonable to hypothesize the existence of a common and essential pathway of molecular signaling that leads to the expression of these stress genes (Fig. 2). The identification and characterization of the transcription factors that regulate the expression of the genes induced by these forms of stress should greatly facilitate our future understanding of the mechanism of stress response.
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PMID:Gene expression in acute myocardial stress. Induction by hypoxia, ischemia, reperfusion, hyperthermia and oxidative stress. 776 Mar 41

In recent years, attempts have been made to increase longevity in animal models (caloric restriction in rodents or overexpression of catalase and superoxide dismutase in transgenic flies, for instance). We report here that flies submitted to hypergravity (3 or 5 g), for 1 or 4 weeks starting from the second day of imaginal life and transferred after that time to 1 g, have a higher resistance to heat shock than flies living continuously at 1 g. Furthermore, male flies that had lived for 2 weeks from the second day of life at 3 or 5 g, lived longer than those living all the time at 1 g; no longevity increase was observed in females. As far as we know, this is the first example in flies showing that a mild stress at a young age not only increases resistance to an acute stress but also increases longevity. A hypothesis to explain these results could be that heat-shock proteins, which are induced by various stress factors, are synthesized in conditions of hypergravity.
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PMID:Increased longevity and resistance to heat shock in Drosophila melanogaster flies exposed to hypergravity. 918 40

Little is known concerning the effect of oxidative stress on the expression of antioxidative enzymes in the decompensated cardiac hypertrophy of spontaneously hypertensive rats (SHR), considered as a model of dilative cardiomyopathy in man. Superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) were characterized in isolated perfused hearts of 18 month old SHR and the age-matched normotensive control Wistar-Kyoto (WKY) rats, before and after 30 min infusion of 25 microM H(2)O(2). After infusion of H(2)O(2), aortic flow decreased in WKY from 26.2 +/- 2.2 to 16.0 +/- 0.8 ml/min (p <.05) but not in SHR (18.2 +/- 1.9 vs. 20.7 +/- 2.2 ml/min). This protection was related to the higher myocardial activities of GPx, MnSOD and CuZnSOD in SHR, compared with those of the WKY group. Although total SOD activity in the SHR fell after H(2)O(2) exposure (to 1.81 +/- 0.13 from 3.56 +/- 0.49 U/mg of protein), catalase activity increased (to 2.46 +/- 0.34 from 1.56 +/- 0.29 k min(-1)mg(-1)protein), compared with the pre-infusion period (p <.05 in each case). In additional studies, hearts were subjected to 30 min of global ischemia followed by 30 min of reperfusion. The results obtained in ischemic/reperfused hearts show the same changes in enzyme activities measured as it was observed in H(2)O(2) perfused hearts, indicating that oxidative stress is independent of the way it was induced. The higher catalase activity derived from elevated mRNA synthesis. The antioxidative system in dilative cardiomyopathic hearts of SHR is induced, probably due to episodes of oxidative stress, during the process of decompensation. This conditioning of the antioxidative potential may help overcome acute stress situations caused by reactive oxygen species in the failing myocardium.
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PMID:Effects of oxidative stress on the expression of antioxidative defense enzymes in spontaneously hypertensive rat hearts. 1103 13

Exposure of Chinese hamster V79 fibroblasts to mild and repetitive H2O2 doses in culture for 15 weeks produced no change in lipid peroxidation status, GSH/GSSG ratio and glutathione peroxidase activity of these cells (VST cells). In contrast, in VST cells catalase levels underwent a prominent increase which could be significantly inhibited and brought down to control levels after treatment with the catalase inhibitor 3-aminotriazole (3-AT). When control (VC) cells were exposed to UV radiation (UVC 5 J/m2) or H2O2 (7.5mM, 15 min), intracellular reactive oxygen species (ROS) levels rose prominently with significant activation of caspase-3. Marked nuclear fragmentation and lower cell viability were also noted in these cells. In contrast, VST cells demonstrated a significantly lower ROS level, an absence of nuclear fragmentation and an unchanged caspase-3 activity after exposure to UVC or H2O2. Cell viability was also significantly better preserved in VST cells than VC cells after UV or H2O2 exposures. Following 3-AT treatment of VST cells, UVC radiation or H2O2 brought about significantly higher elevations in intracellular ROS, increases in caspase-3 activity, significantly lowered cell viability and marked nuclear fragmentation, indicating the involvement of high catalase levels in the cytoprotective effects of repetitive stress. Therefore, upregulation of the antioxidant defense after repetitive oxidative stress imparted a superior ability to cope with subsequent acute stress and escape apoptotic death and loss of viability.
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PMID:Enhancement of catalase activity by repetitive low-grade H2O2 exposures protects fibroblasts from subsequent stress-induced apoptosis. 1294 22

The aim of this study was to investigate the effects of acute, repeated and chronic restraint stress on the antioxidant status and lipid peroxidation. For this purpose, 48 male Wistar rats, aged three months were used in this study. Rats were separated into six groups as follows; control (C), acute stress (AS), restrained for 7 days (1 h/day) (RS), restrained for 21 days (1 h/day) (CS1), restrained for 28 days (1 h/day) (CS2) and restrained for 21 days (1 h/day) and allowed to recovery for 7 days (CS3). Copper, zinc-superoxide dismutase (Cu, Zn-SOD), catalase (CAT) and selenium-dependent glutathione peroxidase (Se-GSH-Px) activities, corticosterone, reduced glutathione (GSH) and thiobarbituric acid-reactive substances (TBARS) levels were measured in blood samples. Corticosterone levels of all groups were found to be elevated after stress compared to group C. Cu, Zn-SOD activity was lower in all stress groups than in group C. CAT and Se-GSH-Px activities were increased in all stress groups. All stress models decreased GSH levels except for the CS3 group. TBARS levels were higher in stress groups than in C group except for AS group. The highest corticosterone level, CAT and Se-GSH-Px activity and TBARS level were seen in group RS. The lowest Cu, Zn-SOD activity and GSH level were seen in group CS2. These results may have an important implication for impaired erythrocyte antioxidant enzyme activities and glutathione levels resulting from exposure to different stress models (acute, repeated and chronic restraint stress).
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PMID:Marked changes in erythrocyte antioxidants and lipid peroxidation levels of rats exposed to acute, repeated and chronic restraint stress. 1563 87

Chronic exposure to stress alters the prooxidant-antioxidant balance, which might lead to the development of various human pathological states. In order to explain the role of antioxidant response in stress-induced injury, we examined the effects of two types of acute stress, as well as combined effects of chronic and acute stress on manganese-superoxide dismutase, copper,zinc-superoxide dismutase, and catalase activities in rat brain hippocampus. Our results show that chronic stress induces an increase in oxidative enzyme activities and that adaptation to chronic stress might alter hippocampal antioxidant mechanisms' response to acute stress.
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PMID:Antioxidant enzyme activity in rat hippocampus after chronic and acute stress exposure. 1615 56

The study deals with activity of three antioxidant enzymes, copper, zinc-superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD), catalase (CAT) in hippocampus of rats, following the exposure to single chronic (individual housing or forced swimming) and acute (immobilization or cold) stress, as well as to combined chronic/acute stress. In addition, plasma noradrenaline (NA) and adrenaline (A) concentrations were measured in the same stress conditions, because their autooxidation can add to the oxidative stress. We observed that i) long-term social isolation and repeated forced swimming had minor effects on plasma catecholamines, but in the long-term pretreated groups, acute stressors caused profound elevation NA and A levels, ii) chronic stressors activate antioxidant enzymes, iii) acute stressors decrease catalase activity, their effects on CuZnSOD appear to be stressor-dependent, whereas MnSOD is not affected by acute stressors, and iv) pre-exposure to chronic stress affects the antioxidant-related effects of acute stressors, but this effect depends to a large extent on the type of the chronic stressor. Based on both metabolic and neuroendocrine data, long-term isolation appears to be a robust psychological stressor and to induce a "priming" effect specifically on the CuZnSOD and CAT activity.
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PMID:Alterations in hippocampal antioxidant enzyme activities and sympatho-adrenomedullary system of rats in response to different stress models. 1623 59

Stress can be viewed as a cause of adverse circumstance that induces a wide range of biochemical and behavioral changes. Oxidative stress is a major contributor to the genesis of neurodegenerative and neuropsychiatric problems. In the present study, we investigated the protective effect of alprazolam in acute immobilization-induced various behavioral and biochemical alteration in mice. Mice were immobilized for a period of 6 h. Alprazolam (0.25 and 0.5 mg/kg, i.p.) was administered 30 min before subjecting the animals to acute stress and several behavioral (mirror chamber, actophotometer, tail flick test) and biochemical tests (malondialdehyde level, glutathione, catalase, nitrite and protein) were performed. Acute immobilization stress for a period of 6 h caused severe anxiety, analgesia and decreased locomotor activity in mice. Biochemical analyses revealed an increase in malondialdehyde, nitrite level and depleted glutathione and catalase activity in stressed brain. Pretreatment with alprazolam (0.25 and 0.5 mg/kg, i.p.) significantly reversed immobilization stress-induced anxiety, analgesia and impaired locomotor activity. Biochemically, alprazolam pretreatment decreased malondialdehyde, nitrite activity and restored reduced glutathione level and catalase activity. These results suggest that alprazolam has a neuroprotective effect and can be used in the treatment and management of stress and related disorders.
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PMID:Protective effect of alprazolam in acute immobilization stress-induced certain behavioral and biochemical alterations in mice. 1765 28

Angiotensin II (Ang II) induces reactive oxygen species (ROS) production by human vascular smooth muscle cells (hVSMCs). ROS have been implicated in the development of both acute stress-induced premature senescence (SIPS) and chronic replicative senescence. Global oxidative DNA damage triggers SIPS and telomere DNA damage accelerates replicative senescence, both mediated via p53. This study tests the hypothesis that DNA is an important target for Ang II-induced ROS leading to senescence via telomere-dependent and independent pathways. DNA damage was quantified using the Comet assay, telomere DNA length by Southern blotting and hVSMC senescence by senescence-associated beta-galactosidase staining. Exposure to Ang II increased DNA damage in hVSMCs within 4 hours. Inhibition by an AT1 receptor antagonist (losartan metabolite: E3174) or catalase, confirmed that Ang II-induced DNA damage was AT1 receptor-mediated, via the induction of ROS. Acute exposure to Ang II resulted in SIPS within 24 hours that was prevented by coincubation with E3174 or catalase. SIPS was associated with increased p53 expression but was not dependent on telomere attrition because overexpression of human telomerase did not prevent Ang II-induced SIPS. Exposure to Ang II over several population doublings accelerated the rate of telomere attrition (by >2-fold) and induced premature replicative senescence of hVSMCs--an effect that was also attenuated by E3174 or catalase. These data demonstrate that Ang II-induced ROS-mediated DNA damage results in accelerated biological aging of hVSMCs via 2 mechanisms: (1) Acute SIPS, which is telomere independent, and (2) accelerated replicative senescence which is associated with accelerated telomere attrition.
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PMID:Angiotensin II-mediated oxidative DNA damage accelerates cellular senescence in cultured human vascular smooth muscle cells via telomere-dependent and independent pathways. 1799 83

Acute stress has been known to produce several behavioral, neurochemical and biochemical alterations. Cyclooxygenase (COX) enzymes are involved in pathogenesis of several brain disorders including Alzheimer disease, epilepsy, depression, in addition to pain and inflammation. In the present study, we examined the role of non-selective (naproxen) and selective (rofecoxib, valdecoxib) COX-2 inhibitors against acute immobilization stress-induced behavioral alterations and oxidative damage in mice. Mice were subjected to acute immobilization stress for a period of 6 h. Naproxen (7 and 14 mg/kg, ip), rofecoxib (5 and 10 mg/kg, ip) or valdecoxib (5 and 10 mg/kg, ip) were administered 30 min before acute stress. Six-our immobilization stress significantly caused anxiety-like behavior, memory deficit and impaired motor activity as well as oxidative damage (raised lipid peroxidation, nitrite activity, depletion of reduced glutathione and catalase activity) as compared to naive animals placed on sawdust (p < 0.05). Pretreatment with naproxen (7 and 14 mg/kg, ip), rofecoxib (5 and 10 mg/kg, ip) and valdecoxib (5 and 10 mg/kg, ip) significantly improved locomotor activity, antianxiety effect, memory retention (memory deficit) and attenuated oxidative damage (lowering of raised malondialdehyde, nitrite activity, restoration of reduced glutathione and catalase activity as compared to immobilization stress group (p < 0.05). Results suggest the neuroprotective and antioxidant effect of both non-selective and selective COX-2 inhibitors.
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PMID:Protective effect of non-selective and selective COX-2-inhibitors in acute immobilization stress-induced behavioral and biochemical alterations. 1819 59


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