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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is an attempt to find a teleological rationale for the involution of the thymus with aging. The thymus is the first organ in the body to age, which seems incongruent considering its cardinal role in the immune system. An analogical incongruency can be seen in the fact that acute stress is generally accompanied by a reversible involution of the thymus. We hypothesized earlier, that this reversible involution might protect the organism from the danger of autoimmune diseases. It stands to reason that, in nature, conditions leading to stress frequently entail massive tissue destruction. This may cause the appearance of "altered self" components, leading to the formation of autoantibodies. Hence, the temporary shut-off of thymic activity would be beneficial. A similar argument holds in the case of aging and will be elaborated as follows: 1) Formation of antibodies per se entails the danger of autoimmune mechanisms, hence the process is controlled at various levels; 2) The aging process is characterized by the increasing appearance of non-self components as a result of DNA errors and post-translational changes due to free radicals and other high energy oxygen derivatives; 3) Early involution serves, in our opinion, to reduce the risk of autoimmune diseases which increases with aging, and should therefore be regarded as an adaptation of the organism to aging; 4) If this notion proves to be correct the desirability of restoring full thymic activity in old people becomes questionable.
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PMID:Hypothesis: involution of the thymus with aging--programmed and beneficial. 192 91

We investigated the effects of acute and chronic stress on the DNA synthesis of the gastroduodenal mucosa of the rat using two different methods of physical stress at various time intervals. Acute stress was produced in the rats being briefly plunged or swimming for two hours (water temperature 37 degrees C). "Sham - transported" rats were used as controls. The results indicate that in the stomach the DNA synthesis was substantially reduced during acute stress in both groups tested (when compared to controls). The DNA synthesis was also reduced in experimental rats after one and two weeks of stress (as compared to day one). By four and eight weeks, the rate of DNA synthesis in the gastric mucosa had significantly increased in the stressed animals. Controls demonstrated significantly lower DNA values following two to eight weeks of stress (as compared to day one). From the outset, the DNA replication values were 2.5 to 3 times higher in the duodenal mucosa than in the gastric mucosa. Following two weeks of stress, the duodenal mucosa of both test groups showed significantly lower DNA values than controls, but significantly higher values after four weeks of stress. By eight weeks, the duodenal mucosa in all rats had reached the same values as that of day one. This was considered a sign of "adaptation to stress" in the duodenal mucosa. The above results suggest that the fluctuations of DNA replication may be connected to compensatory mechanisms aimed at adjusting the gastroduodenal mucosa to protracted stress situations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:DNA synthesis in the gastroduodenal mucosa during acute and chronic stress in the rat. 297 30

The enhancement of tumor development following acute stress has been demonstrated in some animal studies. This study was designed to explore mechanisms that would account in part for the relationship between stress and tumor development at the level of DNA repair, using a rat model. Forty-four rats were given the carcinogen dimethylnitrosamine in their drinking water, and half were randomly assigned to a rotational stress condition. The levels of methyltransferase, a DNA repair enzyme induced in response to carcinogen damage, were significantly lower in spleens from the stressed animals. These data suggest that stress may impair DNA repair.
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PMID:Effects of stress on methyltransferase synthesis: an important DNA repair enzyme. 407 16

Recently progress has been made on O2 toxicity and pathology related to numerous environmental contaminants in insects. The pro-oxidants studied included: dioxin, paraquat, and an assorted array of quinones, 8-methoxypsorlen, arsenic, and mercury. The responses to these oxidants are diverse, but they arise from the reactive oxygen species. These pro-oxidants in insects cause lipid peroxidation, protein and enzyme oxidation, and GSH depletion. Potentially, they may also cause DNA oxidation, and form DNA adducts. Oxidative challenge is alleviated by antioxidant compounds, but more importantly by the induction of antioxidant enzymes, which are crucial for the termination of O2 radical cascade and lipid peroxidation chain reaction. Insects exhibit a wasting syndrome under sub-acute stress. In acute toxicity vital physiological processes impaired are hemolymph melanization and diuresis. Thus, insects resemble vertebrates in both the response to oxidative stress and its pathological consequences. These results raise the prospect that insects may serve as non-mammalian model species for monitoring the oxidative-stress component of environmental toxicity.
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PMID:Oxidative stress from environmental pollutants. 760 41

The aim of this study was to examine the influence of acute stress on the realization of the effects of estrogens in the uterus of ovariectomized rats. The rats were immobilized for 6 h and given a single injection of estradiol dipropionate (E2; 10 micrograms/rat, i.m.). E2-only treated rats, olive oil injected and stressed rats, olive oil-only treated rats and untreated ovariectomized animals were used as controls. The effect of E2 was assessed by the volumes of cells, nuclei and nucleouli (morphometry), DNA content (Feulgen technique) and proliferative activity (mitotic index) in luminal epithelium, in glandular epithelium and in stromal cells of endometrium 24, 36 and 48 h after the injection of E2 or olive oil. All the effects of E2 were reduced in E2-treated rats subjected to stress in all the uterine structures. In olive oil treated rats, stress induced certain increase in the volume of cells and nuclei and slight increase in the DNA content in all the structures. It is suggested that the influence of stress on the uterus is mediated by impairment of some septs in the mechanism of action of estrogen on the uterus, which leads to a decrease in the sensitivity of the uterine structures to estrogens. Without estrogen stimulation the effect of stress on the uterus is realized via estrogen-independent pathways.
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PMID:Realization of estradiol effects in the uterus of ovariectomized rats under acute stress. 763 35

Reactive oxygen species (ROS) are implicated in the pathogenesis of stress-induced gastrointestinal mucosal injury. In the present study, we have investigated the effects of acute and chronic stress on the enhanced production of ROS including superoxide anion [SA; as determined by cytochrome c reduction (CCR)] and hydroxyl radicals (OH), and correlated the enhanced production of these free radicals with increased lipid peroxidation, membrane microviscosity and DNA fragmentation, indices of oxidative tissue damage, in the gastric and intestinal mucosa of female Sprague-Dawley rats. Furthermore, the protective ability of bismuth subsalicylate (BSS) against the gastrointestinal mucosal injury induced by acute and chronic stress was determined. Acute stress was induced for a period of 90 min, while chronic stress was induced for 15 min/day for 15 consecutive days. Half of the animals exposed to acute stress were pretreated orally with 15 mg BSS/kg 30 min prior to the exposure to acute stress. Similarly, half of the animals exposed to water-immersion restraint chronic stress were pretreated orally with 7.5 mg BSS/kg/day for 15 consecutive days 30 min prior to the exposure to chronic stress. Acute stress produced greater injury to both gastric and intestinal mucosa as compared to chronic stress. Acute stress increased CCR and OH production by 10.0- and 14.3-fold, respectively, in the gastric mucosa, and 10.4- and 17.0-fold, respectively, in the intestinal mucosa. Pretreatment with BSS prevented the acute stress-induced increase in CCR and OH production. Acute stress increased lipid peroxidation, DNA fragmentation and membrane microviscosity by 3.6-, 4.0- and 11.6-fold, respectively, in gastric mucosa, and 4.1-, 5.0- and 16.2-fold, respectively, in intestinal mucosa. BSS decreased acute stress-induced lipid peroxidation, DNA fragmentation and membrane microviscosity by approximately 26, 35 and 30%, respectively, in gastric mucosa, and by 20, 36 and 30%, respectively, in the intestinal mucosa. Chronic stress increased CCR and OH production by 4.8- and 6.3-fold, respectively, in gastric mucosa, and 4.6- and 6.9-fold, respectively, in intestinal mucosa. Chronic stress increased lipid peroxidation and DNA fragmentation by 2.9- and 3.3-fold, respectively, in gastric mucosa, and 3.3- and 4.2-fold, respectively, in intestinal mucosa. BSS decreased chronic stress-induced lipid peroxidation, DNA fragmentation and membrane microviscosity by approximately 41, 44 and 45%, respectively, in gastric mucosa, and by 39, 52 and 51%, respectively, in the intestinal mucosa. Daily administration of BSS provided greater protection against chronic stress-induced oxidative gastrointestinal injury as compared to the acute stress. These results demonstrate that both acute and chronic stress can induce gastrointestinal mucosal injury through enhanced production of ROS, and that BSS can significantly protect against gastrointestinal mucosal injury.
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PMID:Acute and chronic stress-induced oxidative gastrointestinal mucosal injury in rats and protection by bismuth subsalicylate. 1044 9

Neuronal mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) proteins are glucocorticoid-activated transcription factors that bind identical DNA response elements yet transduce distinct physiological/transcriptional actions. The present study assessed regulation of adrenocorticosteroid receptor RNA and protein following intermittent stress exposure, using Sprague Dawley (S-D) and stress-hyperresponsive Fischer 344 (F344) rat strains. The F344 (but not S-D) strain showed enhanced acute stress responsivity and enhanced corticosterone secretion following prolonged stress. F344 rats also showed reduced responsiveness to a novel stressor after prolonged stress exposure, suggestive of enhanced glucocorticoid negative feed-back. Upon prolonged stress, F344 rats down-regulated MR hnRNA in CA1, CA3, and dentate gyrus. Transcriptional changes were accompanied by decreased expression of the alpha 5' messenger RNA (mRNA) form, consistent with altered promoter utilization. In contrast, alpha 5' splice variant, full-length mRNA, and MR protein expression were not affected by stress in either strain, implying that transcriptional changes do not affect overall mRNA or protein expression. GR protein was increased in pyramidal and granule cell somata/nuclei of F344 rats despite lack of a change in mRNA expression. These data suggest that prolonged stress elicits restricted changes in MR and GR expression in the F344 strain only. Overall, stable expression of adrenocorticosteroid receptors is rigorously defended in hippocampal neurons, apparently through transcriptional and posttranscriptional mechanisms.
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PMID:Defense of adrenocorticosteroid receptor expression in rat hippocampus: effects of stress and strain. 1046 67

To test the hypothesis that the aging mammalian heart and brain might have increased vulnerability to acute stress, DNA fragmentation was studied after hypoxia-reoygenation in young adult (6 months) and old (22-24 months) F344 rats. Heart and brain tissue were examined at the following time points: 30, 60, or 90 min of hypoxia (H, 5% O2, 95% N2) plus 2 h of reoxygenation (R, room air, 21% O2). With increasing duration of hypoxia preceding the reoxygenation, the extent of DNA fragmentation (in situ terminal dUTP nick end labeling, TUNEL, positive cells) was progressively higher in both age groups, greater in the old compared to that of the young adult rat. The levels of the anti-apoptotic proteins bcl-2 and bcl-xL, were similar in young and old at baseline and tended to increase in both age groups after hypoxia/reoxygenation. The pro-apoptotic protein, bax, was higher at baseline in the old; it rose after hypoxia/reoxygenation in the young adult heart and brain, but was unchanged in the old heart and was decreased in the old brain. The ratios of bcl-2/bax and of bcl-xL/bax were higher in the old heart and brain compared to that in the young adult after hypoxia/reoxygenation. Thus, compared to that of the young adult, the heart and brain of the old rat have lower thresholds and are more vulnerable to injury induced by hypoxia/reoxygenation, despite rapid and heightened expression of the anti-apoptotic proteins bcl-2 and bcl-xl. This could be due partly to the age-associated increase in the basal expression of the pro-apoptotic protein bax, as well as possibly other factors.
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PMID:Influence of age on hypoxia/reoxygenation-induced DNA fragmentation and bcl-2, bcl-xl, bax and fas in the rat heart and brain. 1065 80

The unfolded protein response (UPR) regulates gene expression in response to stress in the endoplasmic reticulum (ER). We determined the transcriptional scope of the UPR using DNA microarrays. Rather than regulating only ER-resident chaperones and phospholipid biosynthesis, as anticipated from earlier work, the UPR affects multiple ER and secretory pathway functions. Studies of UPR targets engaged in ER-associated protein degradation (ERAD) reveal an intimate coordination between these responses: efficient ERAD requires an intact UPR, and UPR induction increases ERAD capacity. Conversely, loss of ERAD leads to constitutive UPR induction. Finally, simultaneous loss of ERAD and the UPR greatly decreases cell viability. Thus, the UPR and ERAD are dynamic responses required for the coordinated disposal of misfolded proteins even in the absence of acute stress.
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PMID:Functional and genomic analyses reveal an essential coordination between the unfolded protein response and ER-associated degradation. 1084 80

The precise mechanisms by which beneficial responses to acute stress are transformed into long-term pathological effects of chronic stress are largely unknown. Western blot analyses revealed that members of the AP1 transcription factor family are differentially regulated by single and repeated stress in the rat adrenal medulla, suggesting distinct roles in establishing stress-induced patterns of gene expression in this tissue. The induction of c-fos was transient, whereas marked elevation of long-lasting Fos-related antigens, including Fra2, was observed after repeated immobilization. We investigated DNA protein interactions at the AP1-like promoter elements of two stress-responsive genes, tyrosine hydroxylase and dopamine beta-hydroxylase. Increased DNA-binding activity was displayed in adrenomedullary extract from repeatedly stressed rats, which was predominantly composed of c-Jun- and Fra2-containing dimers. The induction of Fra2 and increased AP1-like binding activity was reflected in sustained transcriptional activation of tyrosine hydroxylase and dopamine beta-hydroxylase genes after repeated episodes of stress. The functional link between Fra2 and regulation of tyrosine hydroxylase and dopamine beta-hydroxylase transcription was confirmed in PC12 cells coexpressing this factor and the corresponding promoter-reporter gene constructs. These studies emphasize the potential importance of stress-evoked increases in the expression of the Fra2 gene for in vivo adaptations of the adrenal catecholamine producing system.
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PMID:Fos-related antigen 2: potential mediator of the transcriptional activation in rat adrenal medulla evoked by repeated immobilization stress. 1090 2


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