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)

Oxidative stress is a major contributor to the alterations of various pathological conditions, including neurodegenerative and neuropsychiatric problems. Antioxidative flavonoids, ubiquitously included in vegetables, fruits, and teas, are expected to prevent degenerative diseases. Recently, flavonoids have been characterized as neuroprotectants in the treatment of various neurological disorders. The present study was designed to investigate protective effects of quercetin, a bioflavonoid, against acute immobilization-induced behavioral and biochemical alterations in mice. Mice were immobilized for a period of 6 hours. Quercetin (20 and 40 mg/kg, i.p.) was administered 30 minutes before subjecting the animals to acute stress. Behavioral tests (mirror chamber, actophotometer, and tail flick test) and biochemical analysis (malondialdehyde, reduced glutathione, catalase, nitrite, and protein levels) were subsequently performed. Acute immobilization stress for a period of 6 hours caused severe anxiety, analgesia, and impaired motor activity in mice. Biochemical analyses revealed an increase in malondialdehyde and nitrite levels as well as partial depletion of reduced glutathione and catalase activity in immobilization-stressed brain. Behavioral and biochemical parameters were significantly altered as compared to naive mice. Pretreatment with quercetin (20 and 40 mg/kg, i.p.) significantly reversed immobilized stress-induced anxiety and analgesia and reduced locomotor activity. Biochemically, quercetin treatment attenuated malondialdehyde accumulation and nitrite activity and restored the depleted reduced glutathione and catalase activity. Neuroprotective effects of quercetin were significantly improved as compared to control (immobilized stressed) animals. Results suggest that neuroprotective properties of quercetin can be used in the treatment and management of stress and related disorders.
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PMID:Quercetin protects against acute immobilization stress-induced behaviors and biochemical alterations in mice. 1880 Aug 93

Frequent and persistent stressful events caused depressive illness. Stress is an aversive stimulus which disturbs physiological homeostasis and reflects a variety of biological systems. The present study was designed to investigate the nitric oxide mechanism in the protective effect of imipramine and venlafaxine against acute immobilization stress-induced behavioral and biochemical alterations in mice. Mice were immobilized for 6h. Imipramine (10 and 20mg/kg) and venlafaxine (5 and 10mg/kg) were administered 30min before subjecting the animals to acute stress. Behavioral tests (mirror chamber, actophotometer, tail flick test) and biochemical analysis (malondialdehyde level, nitrite, glutathione and catalase enzyme) were performed subsequently. Acute immobilization stress caused anxiety like behavior, analgesia, impaired locomotor activity and oxidative stress as compared to naive. Pretreatment with imipramine (10 and 20mg/kg) and venlafaxine (5 and 10mg/kg) significantly reversed immobilized stress-induced behavioral and biochemical alterations. l-arginine (100mg/kg) pretreatment with imipramine (10mg/kg) and venlafaxine (5mg/kg) significantly attenuated the protective effect of imipramine and venlafaxine. However, l-NAME (10mg/kg) and/or methylene blue (10mg/kg) pretreatment with lower dose of imipramine and venlafaxine significantly potentiated their protective effects which were significant as compared to their effect per se respectively. Present study highlights the involvement of nitric oxide mechanism in the protective effect of imipramine and venlafaxine against acute immobilization-induced behavioral and biochemical alterations in mice.
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PMID:Nitric oxide mechanism in protective effect of imipramine and venlafaxine against acute immobilization stress-induced behavioral and biochemical alteration in mice. 1981 80

Sirt1, a NAD-dependent protein deacetylase, is reported to regulate intracellular metabolism and attenuate reactive oxidative species (ROS)-induced apoptosis leading to longevity and acute stress resistance. We created transgenic (TG) mice with kidney-specific overexpression of Sirt1 using the promoter sodium-phosphate cotransporter IIa (Npt2) driven specifically in proximal tubules and investigated the kidney-specific role of Sirt1 in the protection against acute kidney injury (AKI). We also elucidated the role of number or function of peroxisome and mitochondria in mediating the mechanisms for renal protective effects of Sirt1 in AKI. Cisplatin-induced AKI decreased the number and function of peroxisomes as well as mitochondria and led to increased local levels of ROS production and renal tubular apoptotic cells. TG mice treated with cisplatin mitigated AKI, local ROS, and renal tubular apoptotic tubular cells. Consistent with these results, TG mice treated with cisplatin also exhibited recovery of peroxisome number and function, as well as rescued mitochondrial function; however, mitochondrial number was not recovered. Immunoelectron microscopic findings consistently demonstrated that the decrease in peroxisome number by cisplatin in wild type mice was restored in transgenic mice. In HK-2 cells, a cultured proximal tubule cell line, overexpression of Sirt1 rescued the cisplatin-induced cell apoptosis through the restoration of peroxisome number, although the mitochondria number was not restored. These results indicate that Sirt1 overexpression in proximal tubules rescues cisplatin-induced AKI by maintaining peroxisomes number and function, concomitant up-regulation of catalase, and elimination of renal ROS levels. Renal Sirt1 can be a potential therapeutic target for the treatment of AKI.
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PMID:Kidney-specific overexpression of Sirt1 protects against acute kidney injury by retaining peroxisome function. 2013 70

Diabetes mellitus increases susceptibility to acute gastric injury and impairs ulcer healing. Pioglitazone as an agonist of peroxisome proliferator-activated receptor gamma (PPARgamma) is used as anti-diabetic drug and has additionally gastroprotective activities. However, the effect of pioglitazone on the protection and healing of gastric mucosa under diabetic conditions is poorly understood. The aim of the present study was: 1) to compare the effects of treatment with PPARg ligand (pioglitazone) on healing of acetic acid-induced gastric ulcers and prevention of acute water immersion and restraint stress (WRS)-induced gastric lesions in normal rats and those with streptozotocin (STZ)-induced diabetes mellitus; 2) to assess the effects of pioglitazone on the mRNA expression of cyclooxygenase-2 (COX-2), c-NOS, interleukin-1beta and hypoxia inducible factor-1 alpha (HIF-1alpha) in the gastric mucosa of rats with or without STZ-induced diabetes mellitus; 3) to investigate the involvement of endogenous NO and proinflammatory cytokines (IL-1beta, TNF-alpha) in healing of chronic gastric ulcers and in prevention of acute stress lesions by pioglitazone in rats with or without STZ-induced diabetes mellitus. Diabetes was induced in rats by single injection of STZ (70 mg/kg i.p.) four weeks prior to production of gastric ulcers by acetic acid method or induction of stress lesions by 3.5 hours of WRS. Non-diabetic rats were used as controls. Two major animal groups (A and B) were tested; A) diabetic and non-diabetic rats with chronic gastric ulcers treated with 1) pioglitazone (40 mg/kg-d i.g.), 2) pioglitazone in combination of blocker of NO synthase (L-NNA 20 mg/kg-d i.p.), and 3) saline (vehicle-control); and B) diabetic and non-diabetic rats exposed to 3.5 hours of WRS and pretreated with 1) pioglitazone (40 mg/kg i.g.), 2) pioglitazone in combination of blocker of NO synthase (L-NNA 20 mg/kg i.p.), and 3) saline (vehicle-control). The gastric mucosal blood flow was assessed by H(2)-gas clearance method. The area of chronic acetic acid ulcers and number of acute WRS-induced gastric lesions were assessed by planimetry or by counting of number of lesions, respectively. In rats with chronic ulcers, the mRNA expression of HIF-1alpha, IL-1beta and COX-2 was assessed by RT-PCR and protein expression of platelet endothelial cell adhesion molecule-1 (PECAM-1), COX-2 and cNOS was examined by Western blot. In rats with stress lesions, the protein expression of COX-2, cNOS, catalase, PPAR and heat shock protein 70 (HSP70) was examined by Western blot. In diabetic rats, a marked delay in ulcer healing and increased susceptibility to WRS lesions were observed and these effects were accompanied by a significant decrease in GBF. Pioglitazone significantly increased healing of chronic gastric ulcers and exerted a strong protective effect against WRS-induced lesions, but these effects were attenuated by NO-inhibition with L-NNA. Interestingly, the ulcer healing and gastroprotective effects of pioglitazone were weak under diabetic conditions, and this effect on ulcer healing was accompanied by impaired angiogenesis due to decreased PECAM-1 expression, attenuated expression of COX-2 and the increased expression of proinflammatory cytokines compared to those in diabetic rats treated with vehicle. We conclude that: 1) experimental diabetes in rats impairs healing of chronic ulcers and enhances acute stress lesions due to an increase in the expression and release of proinflammatory cytokines such as TNF-alpha and IL-1beta; 2) the ulcer healing effect of pioglitazone, which is, at least in part, mediated by endogenous NO, is significantly attenuated by L-NNA in diabetic rats despite increased COX-2 expression at the ulcer edge; 3) the formation of acute gastric lesions induced by WRS is also attenuated by pretreatment with pioglitazone due to increased GBF probably mediated by NO, as the administration of L-NNA reversed, in part, the preventive action induced by this PPARgamma ligand, and 4) pioglitazone is effective both in healing of chronic ulcers and protection against WRS lesions though its action under diabetic conditions seems to be attenuated, possibly due to reduction in NOS-NO system, angiogenesis and increased expression and release of proinflammatory cytokines.
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PMID:Gastric ulcer healing and stress-lesion preventive properties of pioglitazone are attenuated in diabetic rats. 2081 70

Emotional stress can be viewed as a cause of adverse circumstances that induces a wide range of biochemical and behavioural changes. Oxidative stress is a critical route of damage in various psychological stress-induced disorders such as depression. Antidepressants are widely prescribed to treat these conditions; however, no animal study has investigated the effect of selective serotonin reuptake inhibitors (SSRIs) on the levels of intracellular reactive oxygen species in peripheral blood leucocytes of stressed mice. In this study, mice were immobilized for a period of 6 hr. Fluoxetine (5 mg/kg of body-weight) was administered 30 min. before subjecting the animals to acute stress. The level of intracellular reactive oxygen species in leucocytes of the peripheral blood of stressed mice was investigated using a 2',7'-dichlorofluorescein diacetate probe, and the antioxidant response of fluoxetine was evaluated by superoxide dismutase, diaphorase, catalase and reduced glutathione. Our results show that restraint stress significantly increases the generation of reactive oxygen species in the peripheral defence cells. Treatment with fluoxetine partially reverses the adverse effects of stress. The improvement in cellular oxidative status may be an important mechanism underlying the protective pharmacological effects of fluoxetine, which are clinically observed in the treatment of depressive disorders.
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PMID:Effects of fluoxetine on the oxidative status of peripheral blood leucocytes of restraint-stressed mice. 2162 59

The present study was to investigate the effects of dietary microencapsulated sodium butyrate (SB) and acute pre-slaughter stress, mimicked by subcutaneous corticosterone (CORT) administration, on BW, carcass characteristics, muscle antioxidant status, and meat quality of broiler chickens. A total of 120 1-d-old broiler chickens were fed a control diet (without SB) or a 0.4-g microencapsulated SB/kg diet. On 42 d, half of the birds from each treatment were given 1 single subcutaneous injection of CORT (4 mg/kg of BW in corn oil) to mimic acute stress, whereas the other half were injected with the same amount of corn oil (sham control). Three hours later, BW loss was determined and breast meat samples were collected. The results showed that the BW of the CORT-challenged groups lost much more than the sham control group (P < 0.001), whereas it was alleviated by the dietary microencapsulated SB (P < 0.05). Meanwhile, the catalase activity was decreased and malondialdehyde level was increased by the stress (P < 0.05), and the microencapsulated-SB diet significantly inhibited this effect (P < 0.05). Lower pH values and higher yellowness values were also observed in CORT-challenged chickens (P < 0.05), and the microencapsulated-SB diet treatment partially exerted a preventive effect. Microencapsulated SB significantly decreased the contents of saturated fatty acids and C18:0 (P < 0.01 and P < 0.001), and increased C20:0 and C20:4 contents. However, the effect of the stress treatment on fatty acid composition was insignificant (P > 0.05). In addition, diet and stress did not significantly influence carcass characteristics and the chemical composition of breast meat (P > 0.05). These results suggest that microencapsulated SB was favorable for chickens in the presence of stress, which may be partially ascribed to the ability of SB to decrease catabolism and oxidative injury of tissues.
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PMID:Dietary sodium butyrate alleviates the oxidative stress induced by corticosterone exposure and improves meat quality in broiler chickens. 2201 Feb 46

Stress is associated with detrimental effects on male reproductive function. It is known that stress increases reactive oxygen species (ROS) generation in the male reproductive tract. High ROS levels may be linked to low sperm quality and male infertility. However, it is still not clear if ROS are generated by stress in the testis. The objective of this study was to characterize the role of oxidative stress induced by cold-water immersion stress in the testis of adult male rats and its relation with alterations in cauda epididymal sperm. Adult male rats were exposed to acute stress or chronic stress by cold-water immersion. Rats were sacrificed at 0, 6, 12, and 24 hours immediately following acute stress exposure, and after 20, 40, and 50 days of chronic stress. ROS production increased only at 6 hours post-stress, while the activity and expression of antioxidant enzymes, lipid peroxidation (LPO), and sperm parameters were not modified in the testis. Corticosterone increased immediately after acute stress, whereas testosterone was not modified. After chronic stress, testicular absolute weight decreased; in addition, ROS production and LPO increased at 20, 40, and 50 days. The activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) decreased throughout the duration of chronic stress and the activity of catalase (CAT) decreased at 40 and 50 days, and increased at 20 days. The expression of copper/zinc superoxide dismutase (SOD1) and CAT were not modified, but the expression of phospholipid hydroperoxide glutathione peroxidase (GPx-4) decreased at 20 days. Motility, viability, and sperm count decreased, while abnormal sperm increased with chronic stress. These results suggest that during acute stress there is a redox state regulation in the testis since no deleterious effect was observed. In contrast, equilibrium redox is lost during chronic stress, with low enzyme activity but without modifying their expression. In addition, corticosterone increased while testosterone decreased, this decrease is related to the negative effects seen in sperm.
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PMID:Oxidative status in testis and epididymal sperm parameters after acute and chronic stress by cold-water immersion in the adult rat. 2564 May 72

Brest harbor (Bay of Brest, Brittany, France) has a severe past of anthropogenic chemical contamination, but inputs tended to decrease, indicating a reassessment of its ecotoxicological status should be carried out. Here, native and caged mussels (Mytilus spp.) were used in combination to evaluate biological effects of chronic chemical contamination in Brest harbor. Polycyclic aromatic hydrocarbon (PAH) contamination was measured in mussel tissues as a proxy of harbor and urban pollution. Biochemical biomarkers of xenobiotic biotransformation, antioxidant defenses, generation of reducing equivalents, energy metabolism and oxidative damage were studied in both gills and digestive glands of native and caged mussels. In particular, activities of glutathione-S-transferase (GST), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), NADP-dependent isocitrate dehydrogenase (IDP), pyruvate kinase (PK) and phosphoenolpyruvate carboxykinase (PEPCK) were measured and lipid peroxidation was assessed by malondialdehyde (MDA) quantification. In addition, a condition index was calculated to assess the overall health of the mussels. Moderate PAH contamination was detected in digestive glands of both native and caged individuals from the exposed site. Modulations of biomarkers were detected in digestive glands of native harbor mussels indicating the presence of a chemical pressure. In particular, results suggested increased biotransformation (GST), antioxidant defenses (CAT), NADPH generation (IDP) and gluconeogenesis (PEPCK), which could represent a coordinated response against chemically-induced cellular stress. Lipid peroxidation assessment and condition index indicated an absence of acute stress in the same mussels suggesting metabolic changes could, at least partially, offset the negative effects of contamination. In caged mussels, only GR was found modulated compared to non-exposed mussels but significant differences in oxidative stress and energy-related biomarkers were observed compared to native harbor mussels. Overall, these results suggested mussels chronically exposed to contamination have set up metabolic adaptation, which may contribute to their survival in the moderately contaminated harbor of Brest. Whether these adaptive traits result from phenotypic plasticity or genetic adaptation needs to be further investigated.
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PMID:Active and passive biomonitoring suggest metabolic adaptation in blue mussels (Mytilus spp.) chronically exposed to a moderate contamination in Brest harbor (France). 2581 57

It is observed that memories are more strengthened in a stressful condition. Studies have also demonstrated an association between stressful events and the onset of depression and anxiety. Considering the nootropic, anxiolytic and antidepressant-like properties of curcumin in various experimental approaches, we appraised the beneficial effects of this herb on acute immobilization stress-induced behavioral and neurochemical alterations. Rats in test group were administrated with curcumin (200mg/kg/day), dissolved in neutral oil, for 1 week. Both control and curcumin-treated rats were divided into unstressed and stressed groups. Rats in the stressed group were subjected to immobilization stress for 2h. After stress, the animals were subjected to behavioral tests. Immobilization stress induced an anxiogenic behavior in rats subjected to elevated plus maze test (EPM). Locomotor activity was also significantly increased following the acute immobilization stress. Pre-administration of curcumin prevented the stress-induced behavioral deficits. Highest memory performance was observed in stressed rats that were pre-treated with curcumin in Morris water maze (MWM). Brain malondialdehyde (MDA) levels, catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and acetylcholinesterase (AChE) activities were also estimated. Present study suggests a role of antioxidant enzymes in the attenuation of acute stress induced anxiety by curcumin. The findings therefore suggest that supplementation of curcumin may be beneficial in the treatment of acute stress induced anxiety and enhancement of memory function.
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PMID:Pretreatment with curcumin attenuates anxiety while strengthens memory performance after one short stress experience in male rats. 2586 55

BACKGROUND We have explored sex differences in ability to maintain redox balance during acute oxidative stress in brains of mice. We aimed to determine if there were differences in oxidative/antioxidative status upon hyperoxia in brains of reproductively senescent CBA/H mice in order to elucidate some of the possible mechanisms of lifespan regulation. MATERIAL AND METHODS The brains of 12-month-old male and female CBA/H mice (n=9 per sex and treatment) subjected to 18-h hyperoxia were evaluated for lipid peroxidation (LPO), antioxidative enzyme expression and activity - superoxide dismutase 1 and 2 (Sod-1, Sod-2), catalase (Cat), glutathione peroxidase 1 (Gpx-1), heme-oxygenase 1 (Ho-1), nad NF-E2-related factor 2 (Nrf2), and for 2-deoxy-2-[18F] fluoro-D-glucose (18FDG) uptake. RESULTS No increase in LPO was observed after hyperoxia, regardless of sex. Expression of Nrf-2 showed significant downregulation in hyperoxia-treated males (p=0.001), and upregulation in hyperoxia-treated females (p=0.023). Also, in females hyperoxia upregulated Sod-1 (p=0.046), and Ho-1 (p=0.014) genes. SOD1 protein was upregulated in both sexes after hyperoxia (p=0.009 for males and p=0.011 for females). SOD2 protein was upregulated only in females (p=0.008) while CAT (p=0.026) and HO-1 (p=0.042) proteins were increased after hyperoxia only in males. Uptake of 18FDG was decreased after hyperoxia in the back brain of females. CONCLUSIONS We found that females at their reproductive senescence are more susceptible to hyperoxia, compared to males. We propose this model of hyperoxia as a useful tool to assess sex differences in adaptive response to acute stress conditions, which may be partially responsible for observed sex differences in longevity of CBA/H mice.
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PMID:Diminished Resistance to Hyperoxia in Brains of Reproductively Senescent Female CBA/H Mice. 2637 31


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