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PubMed2006

Endothelial response to stress from exogenous Zn2+ resembles that of NO-mediated nitrosative stress, and is protected by MT-1 overexpression.

While nitric oxide (NO)-mediated biological interactions have been intensively studied, the underlying mechanisms of nitrosative stress with resulting pathology remain unclear. Previous studies have demonstrated that NO exposure increases free zinc ions (Zn(2+)) within cells. However, the resulting effects on endothelial cell survival have not been adequately resolved. Thus the purpose of this study was to investigate the role of altered zinc homeostasis on endothelial cell survival. Initially, we confirmed the previously observed significant increase in free Zn(2+) with a subsequent induction of apoptosis in our pulmonary artery endothelial cells (PAECs) exposed to the NO donor N-[2-aminoethyl]-N-[2-hydroxy-2-nitrosohydrazino]-1,2-ethylenediamine. However, NO has many effects upon cell function and we wanted to specifically evaluate the effects mediated by zinc. To accomplish this we utilized the direct addition of zinc chloride (ZnCl(2)) to PAEC. We observed that Zn(2+)-exposed PAECs exhibited a dose-dependent increase in superoxide (O(2)(-).) generation that was localized to the mitochondria. Furthermore, we found Zn(2+)-exposed PAECs exhibited a significant reduction in mitochondrial membrane potential, loss of cardiolipin from the inner leaflet, caspase activation, and significant increases in TdT-mediated dUTP nick end labeling-positive cells. Furthermore, using an adenoviral construct for the overexpression of the Zn(2+)-binding protein, metallothionein-1 (MT-1), we found either MT-1 overexpression or coincubation with a Zn(2+)-selective chelator, N,N,N',N'-tetrakis(2-pyridylmethyl)ethylene-diamide, in PAECs significantly protected the mitochondria from both NO and Zn(2+)-mediated disruption and induction of apoptosis and cell death. In summary, our results indicate that a loss of Zn(2+) homeostasis produces mitochondrial dysfunction, increased oxidative stress, and apoptotic cell death. We propose that regulation of Zn(2+) levels may represent a potential therapeutic target for disease associated with both nitrosative and oxidative stress.

Adenoviridae↗
PubMed2005

Hypoxic stress in diabetic pregnancy contributes to impaired embryo gene expression and defective development by inducing oxidative stress.

We have shown that neural tube defects (NTD) in a mouse model of diabetic embryopathy are associated with deficient expression of Pax3, a gene required for neural tube closure. Hyperglycemia-induced oxidative stress is responsible. Before organogenesis, the avascular embryo is physiologically hypoxic (2-5% O(2)). Here we hypothesized that, because O(2) delivery is limited at this stage of development, excess glucose metabolism could accelerate the rate of O(2) consumption, thereby exacerbating the hypoxic state. Because hypoxia can increase mitochondrial superoxide production, excessive hypoxia may contribute to oxidative stress. To test this, we assayed O(2) flux, an indicator of O(2) availability, in embryos of glucose-injected hyperglycemic or saline-injected mice. O(2) flux was reduced by 30% in embryos of hyperglycemic mice. To test whether hypoxia replicates, and hyperoxia suppresses, the effects of maternal hyperglycemia, pregnant mice were housed in controlled O(2) chambers on embryonic day 7.5. Housing pregnant mice in 12% O(2), or induction of maternal hyperglycemia (>250 mg/dl), decreased Pax3 expression fivefold, and increased NTD eightfold. Conversely, housing pregnant diabetic mice in 30% O(2) significantly suppressed the effect of maternal diabetes to increase NTD. These effects of hypoxia appear to be the result of increased production of mitochondrial superoxide, as indicated by assay of lipid peroxidation, reduced glutathione, and H(2)O(2). Further support of this interpretation was the effect of antioxidants, which blocked the effects of maternal hypoxia, as well as hyperglycemia, on Pax3 expression and NTD. These observations suggest that maternal hyperglycemia depletes O(2) in the embryo and that this contributes to oxidative stress and the adverse effects of maternal hyperglycemia on embryo development.

Animals↗
PubMed2001

Stress and the gastrointestinal tract III. Stress-related alterations of gut motor function: role of brain corticotropin-releasing factor receptors.

Alterations of gastrointestinal (GI) motor function are part of the visceral responses to stress. Inhibition of gastric emptying and stimulation of colonic motor function are the commonly encountered patterns induced by various stressors. Activation of brain corticotropin-releasing factor (CRF) receptors mediates stress-related inhibition of upper GI and stimulation of lower GI motor function through interaction with different CRF receptor subtypes. CRF subtype 1 receptors are involved in the colonic and anxiogenic responses to stress and may have clinical relevance in the comorbidity of anxiety/depression and irritable bowel syndrome.

Animals↗
PubMed2001

Stress and the Gastrointestinal Tract IV. Modulation of intestinal inflammation by stress: basic mechanisms and clinical relevance.

The stress response in a healthy organism is generally viewed as a warning and thus a protective reaction to a threat. However, the response may be deleterious if it is linked to an inflammatory stimulus or if it proceeds an inflammatory event. Prior stress enhances the response to an inflammatory stimulus by a mechanism that is independent of the release of hypothalamic corticotropin-releasing factor (CRF) or arginine vasopressin. Putative mechanisms include an increase in intestinal permeability as well as the release of the proinflammatory neuropeptide substance P. Stress may also reactivate previous inflammation when applied in conjunction with a small luminal stimulus. This reactivation involves increased permeability and requires the presence of T lymphocytes. Inflammatory mediators activate hypothalamic pathways, and a negative feedback loop, mediated by CRF release, has been proposed because animals with impaired hypothalamic CRF responses are more susceptible to inflammatory stimuli. Together, these experimental observations provide insights into the expression of inflammatory disorders in humans, including inflammatory bowel disease and postinfective irritable bowel syndrome.

Animals↗
PubMed2002

Regional arterial stress-strain distributions referenced to the zero-stress state in the rat.

Morphometric and stress-strain properties were studied in isolated segments of the thoracic aorta, abdominal aorta, left common carotid artery, left femoral artery, and the left pulmonary artery in 16 male Wistar rats. The mechanical test was performed as a distension experiment where the proximal end of the arterial segment was connected via a tube to the container used for applying pressures to the segment and the distal end was left free. Outer wall dimensions were obtained from digitized images of the arterial segments at different pressures as well as at no-load and zero-stress states. The results showed that the morphometric data, such as inner and outer circumference, wall and lumen area, wall thickness, wall thickness-to-inner radius ratio, and normalized outer diameter, as a function of the applied pressures, differed between the five arteries (P < 0.01). The opening angle was largest in the pulmonary artery and smallest in thoracic aorta (P < 0.01). The absolute value of both the inner and outer residual strain and the residual strain gradient were largest in the femoral artery and smallest in the thoracic aorta (P < 0.01). In the circumferential and longitudinal direction, the arterial wall was stiffest in the femoral artery and in the thoracic aorta, respectively, and most compliant in the pulmonary artery. These results show that the morphometric and biomechanical properties referenced to the zero-stress state differed between the five arterial segments.

Animals↗
PubMed2002

Urea stress is more akin to EGF exposure than to hypertonic stress in renal medullary cells.

Although urea is considered to be a cell stressor even in renal medullary cells perpetually exposed to this solute in vivo by virtue of the renal concentrating mechanism, aspects of urea signaling resemble that of a peptide mitogen. Urea was compared with epidermal growth factor and hypertonic NaCl or hypertonic mannitol using a large-scale expression array-based approach. The expression profile in response to urea stress more closely resembled that of EGF treatment than hypertonic stress, as determined by hierarchical cluster analysis; the effect of urea+NaCl was equidistant from that of either solute applied individually. Among the most highly urea- and hypertonicity-responsive transcripts were genes that had previously been shown to be responsive to these solutes, validating this approach. Increased expression of the activating transcription factor 3 by urea was newly detected via expression array and confirmed via immunoblot analysis. Earlier, we noted an abrogation of tonicity-dependent gene regulation by urea, primarily in a transient transfection-based model (Tian W and Cohen DM. Am J Physiol Renal Physiol 280: F904-F912, 2001). Here we applied K-means cluster analysis to demonstrate that the genes most profoundly up- or downregulated by hypertonic stress were partially restored toward basal levels in the presence of urea pretreatment. These global expression data are consistent with our earlier biochemical studies suggesting that urea affords cytoprotection in this context. In the aggregate, these data strongly support the hypothesis that the urea effect in renal medullary cells resembles that of a peptide mitogen in terms of the adaptive program of gene expression and in terms of cytoprotection from hypertonicity.

Activating Transcription Factor 3↗
PubMed1993

Contrasting effects of central alpha-1-adrenoreceptor activation on stress-responsive and stress-nonresponsive subpopulations of corticotropin-releasing hormone neurosecretory cells in the rat.

Stimulation of the rat hypothalamopituitary-adrenal axis during stress involves activation of central alpha 1-adrenergic receptors. The subpopulation of corticotropin-releasing hormone (CRH) neurosecretory cells that contains vasopressin (VP) is selectively activated by several types of stress (immobilization, hypoglycemia, and intracerebroventricular, i.c.v., colchicine), and is located in a catecholamine-rich area of the hypothalamic paraventricular nucleus. Therefore, we tested the hypothesis that the CRH+/VP+ subpopulation is selectively activated by central alpha 1-adrenergic receptors. The alpha 1-agonist methoxamine or vehicle alone was injected i.c.v. after habituation of rats to daily injections of vehicle through a chronic i.c.v. cannula. Activation of the CRH+/VP+ and CRH+/VP- subpopulations was measured by quantifying depletion of neurosecretory vesicles from immunocytochemically identified axons in the external zone of the median eminence. The habituated, vehicle-injected sham control group had normal levels of plasma ACTH and corticosterone, but possessed a significantly higher proportion of VP-containing CRH axons than naive animals. This change is similar to what was observed previously in rats subjected to repeated daily stress. I.c.v. methoxamine caused elevations of plasma ACTH and corticosterone and significant depletions of vesicles from the CRH+/VP+ axons at 1 and 2 h after injection, compared to the sham control group. The CRH+/VP- axons, however, displayed significant accumulations of neurosecretory vesicles at the same times after 300 micrograms methoxamine, compared to the sham control group. After 100 micrograms methoxamine, there was no change in the CRH+/VP- axons, compared to the sham control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1981

[Stress and risk of urolith formation. I. The influence of stress on lithogenous urinary substances (author's transl)].

In the present work the influence of stress situations on the concentrations and excretions of lithogenous urinary substances (calcium, oxalic acid, uric acid) has been studied in defined urine portions of 10 calcium oxalate stone patients and 10 normal subjects and the results compared to those of 20 stone patients and 10 normal subjects without stress. Stress may be objectified in the given task. The increase of concentrations and excretions of lithogenous urinary substances indicates an enhanced risk of stone formation. Uric acid is discussed as an agent promoting the calcium oxalate crystallization. New insights on the calcium oxalate stone genesis are gained from the results.

Adult↗
PubMed1982

Stress and the practice of medicine. II. Stressors, stresses, and strains.

Stresses of medical practice, recognized as severe, do not increase morbidity and mortality of physicians due to physical illness; the rates of substance dependence, divorces, and mental illness, however, exceed those in the general population. This study was undertaken to explore the effect of stress on physicians and to determine its role in the personal and occupational parameters of adaptation. 100 physicians of various specialties were randomly chosen and their responses to a standard questionnaire were computer analyzed. The previous hypothesis of the motivation of the choice of medicine as a vocation was explored from the point of view of personality features and responses to stress. All physicians reported considerable compulsivity. Its continuous utilization leads to failure of adaptation apparently responsible for further emotional and mental maladaptation. On the whole, the group under study did not show severe psychopathology equal to what has been reported in many other studies. Theoretical and practical aspects of this study are elucidated in the paper.

Adult↗
PubMed1992

Assessment of life stress events: the etiology and measurement of traumatic stress disorder.

The impact of stressful life events on health has been of considerable interest from a cross-cultural perspective. Examined herein is the etiology and onset of post-traumatic stress disorder with careful review of the diagnostic criteria, current measures used and clinical dimensions of PTSD. Also examined from a cross-cultural perspective is how psychological trauma may be processed by victims of trauma and subsequent approaches both pharmacological and psychotherapeutic to the treatment of post-traumatic stress disorder.

Combat Disorders↗
PubMed2004

Antioxidative stress-associated genes in circulating progenitor cells: evidence for enhanced resistance against oxidative stress.

Adult and embryonic stem cells hold great promise for regenerative medicine. Expression profiling of stem cells revealed a characteristic imprint of genes, so-called "stemness" genes, providing resistance to stress. Circulating progenitor cells with an endothelial phenotype (EPCs) can be isolated from peripheral blood and contribute to neovascularization and endothelial regeneration. We investigated whether EPCs are equipped with an antioxidative defense to provide resistance against oxidative stress. EPCs exhibited a significantly lower basal reactive oxygen species (ROS) concentration as compared with mature umbilical vein endothelial cells (HUVECs). Incubation with H(2)O(2) (500 microM) or the redox cycler LY-83583 (10 microM) profoundly increased the ROS concentration to 3- and 4-fold and induced apoptosis in HUVECs. In contrast, H(2)O(2) and LY-83583 induced only a minor increase in intracellular ROS levels and apoptosis in EPCs. Consistently, the expression of the intracellular antioxidative enzymes catalase, glutathione peroxidase and manganese superoxide dismutase (MnSOD), was significantly higher in EPCs versus HUVECs and human microvascular endothelial cells. In accordance, combined inhibition of these antioxidative enzymes increased ROS levels in EPCs and impaired EPC survival and migration. Taken together, EPCs reveal a higher expression of antioxidative enzymes and, thus, are exquisitely equipped to be protected against oxidative stress consistent with their progenitor cell character.

Apoptosis↗
PubMed1992

[Effects of Kamikihi-To on autonomic imbalances in SART-stressed (repeated cold-stressed) mice].

The effects of Kamikihi-To (KMK), a traditional Chinese medicine, on autonomic imbalances were evaluated in SART-stressed (repeated cold-stressed) mice. These animals exhibited decreases in pain threshold and contraction of duodenum by acetylcholine, and they showed changes in their electrocardiogram and hematological parameters. All symptoms are thought to be caused by dysautonomia. KMK in dosages of 0.5 and 1.0 g/kg were administered to mice once a day for 8 consecutive days. SART stress was induced from the second day. KMK prevented the decrease in the pain threshold and contraction of the duodenum, although it had no effect on the electrocardiographic or hematological changes. KMK had no similar effect on unstressed mice. This data suggests that KMK might be useful for the treatment of clinical autonomic imbalances.

Acetylcholine↗
PubMed1986

Stress and immune responses. IV. Adrenal involvement in the alteration of antibody responses in restraint-stressed mice.

We investigated the correlation between restraint stress-induced alteration of antibody responses and adrenal hormones. Adrenalectomy (Adx) blocked both the suppression of antibody response against T cell-dependent (TD) antigen and the enhancement of that against T cell-independent (TI) antigen in stressed mice. Adx also inhibited the atrophy of both thymus and spleen caused by restraint. Pre-treatment of metyrapone, an inhibitor of adrenocortical steroid biosynthesis, had an effect that was similar to, but far weaker than that of Adx on stressed mice. The pre-administration of phenoxybenzamine, an alpha-adrenergic blocking agent, to mice prevented both the inhibition of antibody response to TD antigen and the decrease in spleen cell number of restrained mice. A similar effect was observed in mice pre-treated with 6-hydroxydopamine, an adrenergic neuron degenerating agent. However, no effects of these two agents were observed on the enhancement of antibody response to TI antigen. The suppressive effect of the antibody response to TD antigen was augmented by the pre-administration of propranolol, a beta-adrenergic blocking agent. These results suggest that the suppression of the function of T cells in restrained mice are attributed to the released adrenocortical and adrenal medullary hormones and activated sympathetic nervous system and that the enhancement of B cell function is due to the adrenocortical hormones.

Adrenal Glands↗
PubMed2003

Stress and vascular responses: atheroprotective effect of laminar fluid shear stress in endothelial cells: possible role of mitogen-activated protein kinases.

Atherosclerosis preferentially occurs in areas of turbulent blood flow and low fluid shear stress, whereas laminar blood flow and high shear stress are atheroprotective. Inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha), stimulate expression of endothelial cell (EC) genes that may promote atherosclerosis. Recent findings suggest a steady laminar blood flow decreases EC apoptosis and inhibits TNF-mediated EC activation. EC apoptosis or activation is suggested to be involved in plaque erosion, which may lead to platelet aggregation. TNF-alpha regulates gene expression in ECs, in part, by stimulating mitogen-activated protein (MAP) kinases, which phosphorylate transcription factors. We hypothesized that steady laminar flow inhibits cytokine-mediated activation of MAP kinases in ECs. To test this hypothesis, we determined the effects of steady laminar flow (shear stress = 12 dynes/cm(2)) on TNF-alpha-stimulated activity of three MAP kinases in human umbilical vein ECs (HUVEC): extracellular signal-regulated kinase (ERK1/2), c-Jun N-terminal kinase (JNK), and p38. TNF-alpha activated ERK1/2, JNK, and p38 maximally at 15 min in HUVEC. Pre-exposing HUVEC for 10 min to flow inhibited TNF-alpha activation of JNK, but showed no significant effect on ERK1/2 or p38 activation. Incubation of HUVEC with PD98059, a specific ERK1/2 inhibitor, blocked the flow-mediated inhibition of TNF activation of JNK. Transfection studies with dominant-negative constructs of the protein kinase MEK5 suggested an important role for big mitogen-activated protein kinase 1 (BMK1) in flow-mediated regulation of EC activation by TNF-alpha. Understanding the mechanisms by which steady laminar flow regulates JNK activation by cytokines may provide insight into the atheroprotective mechanisms induced by laminar blood flow.

Animals↗
PubMed2003

Stress and vascular responses: endothelial dysfunction via lectin-like oxidized low-density lipoprotein receptor-1: close relationships with oxidative stress.

Endothelial dysfunction is associated with pathological vascular conditions including atherosclerosis, hypertension, and diabetes. The oxidatively modified form of low-density lipoprotein (LDL) is recognized as a major cause of endothelial dysfunction in atherogenesis. As the receptor for oxidized LDL in endothelial cells, we have identified the lectin-like oxidized LDL receptor-1 (LOX-1). LOX-1 is up-regulated by products of oxidative stresses and the molecules that induce oxidative stresses. Activation of LOX-1 induces the generation of reactive oxygen species and decreases NO released from endothelial cells. LOX-1 activation further induces the expression of endothelin-1, AT(1) receptor, and cell adhesion molecules. Together with these properties, LOX-1 works as an adhesion molecule for activated platelets and neutrophils. Thus, LOX-1, within the close relationships between oxidative stress generation and response, enhances functional changes in endothelial cells that are relevant to the disturbed vascular homeostasis under pathological settings.

Animals↗
PubMedDate not supplied

Nurse occupational stress research. 5: Sources and determinants of stress.

This article, the fifth in a six-part series, reviews the major sources and determinants of nurse stress. The reviewer identifies a wide range of stress determinants, including work overload, interpersonal relationship problems, role conflict and ambiguity, work vs home, resource shortages and pressure from patients, among others. He makes the point that since successive pieces of research keep highlighting the same nurse stress determinants, it would appear that either those who are responsible for addressing the problems and finding solutions are ignoring the research findings or, if interventions are being implemented, they are not working.

Conflict, Psychological↗
PubMed1996

Enhancement of glucocorticoid receptor-mediated gene expression by cellular stress: evidence for the involvement of a heat shock-initiated factor or process during recovery from stress.

Recent reports have demonstrated the ability of cellular stress to cause a large increase in the maximal levels of steroid receptor-mediated gene expression, a process we refer to as the heat shock potentiation effect (HSPE). In the present work, we have analyzed the time of appearance of the HSPE on the glucocorticoid receptor (GR) of L929 cells stably-transfected with the MMTV-CAT reporter plasmid (LMCAT2 cells). In LMCAT2 cells exposed to heat shock (43 degrees C, 2-h) before addition of 1 microM dexamethasone, the first appearance of HSPE (CAT levels greater than hormone-alone) occurred at 8 h of recovery and continued to increase by 24 h of recovery. Treatment of LMCAT2 cells with 1 microM dexamethasone for 2 h before heat or chemical shock (sodium arsenite) resulted in the same delayed onset pattern for the HSPE. Based on a [35S]methionine assay and tests of L929 cells stably transfected with the constitutive pSV2-CAT reporter, evidence is provided that the delayed appearance of the HSPE is not due to the heat shock block of general protein synthesis or to specific repression of CAT mRNA expression or translation. By using short-term incubations (4 h) with dexamethasone during the recovery period, the peaks of HSPE expression during recovery were determined to be 12-16 h for CAT enzyme activities, and 4-8 h for CAT mRNA expression. Taken together, these results provide evidence that the timing of the HSPE is not dependent on the rate of GR activation, or on the type of stress, but rather on a factor or process that is either synthesized or activated during the recovery period following stress.

Animals↗